Ophthalmology Flashcards

Question

How would you treat anterior uveitis?

Answer 1

Topical steroids/subconjucntivals Cycloplegics - relax ciliary body (reduce pain) and cause dilatation of pupil (stops posterior synechiae from forming). Rarely infective therefore can start treatment whilst awaiting results.

Answer 2

Put steroid in the eyes to reduce the inflammation and reduce any systemic side effects. Local: Raised pressure in the eye which can lead to glaucoma- therefore give drops to prevent this. Cataracts- surgery to fix this- reluctant to do this on younger Px as they lose the accommodation reflex with an artificial lens. Systemic: ``` Osteoporosis Indigestion- gastric ulcers which may bleeds therefore give PPI. Immunosuppression Hair loss Hyperglycaemia Weight gain High dose can lead to avascular necrosis of femur Anxiety HTN Cushingoid features ``` Immunosuppressants take time to work so use steroids in the mean time These have less side effects than steroids

Answer 3

Posterior synechiae Pupillary membrane Ocular HTN/glaucoma- three causes- (1) Steroid drops (2) Build up of cell debris from inflamed BV can block the trabecular mesh work and so the ‘draining system’ (3) Increase in pressure can cause the anterior surface of the iris to stick to the cornea causing peripheral anterior synechiae- blocking the angle and trabecular meshwork. Hypotony- if ciliary body not working properly due to inflammation this causes a reduced pressure, as it can’t produce the aqueous humour. Cataract Cystoid macular oedema Posterior subcapsular cataracts- breadcrumb appearance from steroids More worried about a reduced pressure since can’t do much to fix it, OST you can do is give max steroid drops to reduce inflammation and encourage ciliary body to work.

Answer 4

Usually a penetrating injury of one eye where the iris pigment leaks and mixes with the blood. The body develops an immunity against the iris pigment, and so will attack the other eye since it also contains the iris pigment. The person is at risk of losing the sight in the non injured eye. Treat with steroids and immunosuppressants. The bulk of the antigens are in the injured eye and so although the disease will not be cured, the symptoms will be reduced if this eye is removed.

Answer 5

Cataracts Floaters Swelling of macular- cystoid macular oedema

Answer 6

Local- Periocular steroids Intravitreal steroid implants Systemic- Pulse therapy Oral steroids Immunosuppressants instead of long term steroid use Antibiotic/antifungal/antiviral if infectious cause. NB toxoplasma treated with anti toxoplasma drugs first then treat the inflammation. TB uveitis need to be treated with anti-TB first then steroids CMV retinitis- Normal population have CMV but become infective when immunity is lower I.e. HIV, chemotherapy, steroids.

Answer 7

Calcineurin inhibitiors- tacrolimus, cyclosporin. SE- BP, deranged renal function. Cytotoxic immunosuppressants- methotrexate, azathioprine. SE- Bone marrow suppression, lymphoma. Biologics- Infliximab, rituximab. SE- Infections, autoimmune like syndromes.

Answer 8

The internal carotid. | If a person was stabbed in the eye don’t remove the apparatus.

Answer 9

Born without the greater wing of the sphenoid. Brain bulges out through this area. Pulsatile proptosis

Answer 10

Group of conditions characterised by progressive optic neuropathy with corresponding visual field defects. With/without raised IOP. ``` Types include: Primary open-angle glaucoma Angle closure glaucoma Secondary glaucoma (due to uveitis, trauma etc) Congenital glaucoma ```

Answer 11

Main cause of irreversible blindness worldwide. Damage to optic nerve affects peripheral vision first then total sight loss (Tunnel vision) then end stage complete VF loss. Night vision worsens. In the early stages (before tunnel vision) the pupil responses are normal.

Answer 12

Falling over Bumping into things Use their head more to see things around Night vision becomes worse

Answer 13

(1)Increase in IOP- When we measure pressure we measure the anterior chamber pressure. The ciliary body secretes aqueous humour which provides nutrition for the cornea and removes waste/toxins. This drains from the trabecular meshwork. Problem in the draining system will increase the pressure. (2) Poor blood/O2 supply to the nerve head therefore nerve fibres gradually die. This gives you the optic neuropathy and VF defects, which defines glaucoma. (Nerve fibres die usually as you grow older but higher with glaucoma) NB- Loss of VF demonstrated by cupping. As nerve fibres die, the C:D increases and the BV don't have much support so use the cup as their support.

Answer 14

Open or closed angle glaucoma. Each further divided into primary and secondary. ``` Open angle (More Common)- The angle between the iris and cornea remains wide open, slow blockage of trabecular meshwork over time. Closed angle- Sudden block in trabecular meshwork, decreased size of angle between iris and cornea, sudden increase in IOP. ```

Answer 15

``` Raised IOP Increasing age African, Hispanic, Asian FHx Myopia Diabetes, heart disease, HTN ```

Answer 16

Gradual increase in resistance through the trabecular meshwork à difficult for aqueous humour to flow through the meshwork to exit the eye, hence pressure slowly builds up within the eye Increased pressure in the eye causes cupping of the optic disc – normally the optic cup is less than half the size of the optic disc; in increased intraocular pressure the indent is wider- cupping of the optic disc occurs

Answer 17

Largely asymptomatic Visual loss may occur but central vision is preserved until later in disease Diagnosis via routine ophthalmic examination at optometrists GPs may suspect if they visualise cupped discs during ophthalmoscopy Diagnosis- - Ophthalmoscopy- cupped disc - Visual fields - Intraocular pressure- may or may not be elevated

Answer 18

First line- Prostaglandin analogue eye drop i.e. lantanoprost Second line- beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop More advanced consider surgery/laser

Answer 19

``` Raised IOP Age Far East ethnicity/south East Asian FHx Hypermetropia Adrenergic medications Anticholinergic medications Tricyclic antidepressants eg amitriptyline- anticholinergic effects ```

Answer 20

The iris bulges forward and seals off the trabecular meshwork from the anterior chamber This prevents aqueous humour from being able to drain away This results in continual build up of pressure in the eye, esp in the posterior chamber, which causes pressure behind the iris and worsens the closure of the angle OPHTHALMIC EMERGENCY! Can lead to permanent vision loss

Answer 21

``` Appear generally unwell in themselves Acute onset Red eye Blurred vision Halos around lights Associated headache N&V ``` O/E- red eye, teary, hazy cornea, decreased VA, dilatation of affected pupil, fixed pupil size, firm eyeball on palpation

Answer 22

Immediately admit- if there is a delay to admission do the following - Lie pt on their back w/o pillow - Give pilocarpine eyedrops - Give acetazolamide 500mg orally - Give analgesia and anti-emetic if required In secondary care, various medical options to reduce IOP- - Pilocarpine - Oral or IV acetazolamide - Hyperosmotic agents eg glycerol or mannitol to increase osmotic gradient between the blood and fluid in the eye - Timolol- BB- reduces production of aqueous humour - Dorzolamide- CA inhibitor- reduced production of aqueous humour - Brimonidine- sympathomimetic- reduces production of aqueous humour & increased uveoscleral outflow Definitive treatment- -Laser iridotomy- makes hole in iris to allow aqueous humour to flow from posterior chamber into anterior chamber, relieving pressure that was pushing the iris against the cornea, allows fluid to drain

Answer 23

``` Raised IOP Trauma Topical steroids Ocular inflammation Surgical/iatrogenic ```

Answer 24

Acts on muscarinic receptors in sphincter muscles in iris and causes constriction of pupil Therefore it is a miotic agent Also causes ciliary muscle contraction These 2 effects cause the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork to open up

Answer 25

10-21mmHg Goldmann Applanation Tonometry (GAT)- gold standard test Special device mounted on slit lamp, makes contact with cornea and applies different pressures to the front of the cornea to get an accurate measurement Non-contact tonometry- used by opticians Shooting a puff of air at the cornea and measuring the corneal response to the air, less accurate, but gives helpful estimate for general screening purposes

Answer 26

No But optometrist should examine; - Older age- >60 every 2 years, >70 every year (free through NHS) - FHx of glaucoma- people >40 with first-degree relative with open angle glaucoma have eye test annually (free through NHS) - People >40 of black African family origin- annual eye test (not through NHS)

Answer 27

Incurable Can aim to slow down the progression Aim to reduce IOP, even normal tension glaucoma. Can treat through medical therapy, surgery or laser treatment. Medical therapy- B blockers Timalol. Ocular surgeries Lasers

Answer 28

- Use Beta-blocker like Timolol - Mitotics like pilocarpine in angle closed glaucoma will pull the iris away from the trabecular meshwork to improve drainage of aqueous humour. - Prostaglandin analogue like Xalatan will reduce production of aqueous humour and help with drainage; only take one a day. - Alpha adrenergics like Alphagan will reduce production of aqueous humour. - Carbonic anhydrase inhibitors Adverse reaction to meds, eye drops. Stop the drops and find alternative.

Answer 29

Trabeculoplasty- Increases outflow of aqueous by encouraging pumping of trabecular. -Cyclodiode- Destroys parts of the ciliary body. Used only to provide comfort in the blind eye by reducing IOP. Don't use in healthy eye as can cause vision loss. Goniotomy- Used in children Peripheral Laser Iridotomy- Used in closed angle

Answer 30

Trabeculectomy- Making a different tract for the humour to drain by cutting through the eye. Under the top lid they’ll have a ‘bleb’- Px won’t notice. Don’t use in young Px or uveitis since can scar easily and block the new channel. Iritis Blelbitis Sudden increase/ decrease in IOP.

Answer 31

-Red painful eye -N+V (may be there first) -Blurred vision due to cornea hazy -Halo eyes (esp in subacute closed angle glaucoma where the angle opens and close intermittently) -Corneal Oedema- blue haze around -Fixed and oval pupil Ciliary injection

Answer 32

- Give intraocular injections (subconjunctival) of acetozolamide- for quick reduction in IOP. - Keep them hydrated and check IOP in 30mins then again, should reduce pressure within 1hr. - Cornea should become clearer, now able to examine the eye. - Adjunct topical therapy -Then laser peripheral iridotomy in both eyes, creates a hole in the eye to allow aqueous humour drainage.

Answer 33

Onset? Distance/near? Do you wear glasses? When did you have an eye test last?

Answer 34

Cornea fixed at ~40 diopter Lens (variable) ~20 dioptres Axial length ~23mm (distance from cornea to retina)

Answer 35

Deficiency in refraction leading to blurred vision. Either due to physiological causes -Normal cornea but anomalous axial length. (Most common cause in people who wear glasses) -Anomalous cornea but normal axial length. Or Pathological including corneal transplant, rubbing eyes, as result of corneal ulcer etc.

Answer 36

Myopia either normal cornea but longer axial length (common) or high power cornea but normal axial length. Hypermetropia- opposite to myopia. Astigmatism- rugby ball cornea, have two curves in the cornea 90 degrees to each other resulting in blurred vision. Each curve produces its own image. Usually have in both eyes, won’t know unless Px is assessed. Acquired astigmatism I.e. in corneal transplant.

Answer 37

Natural decline in accommodation reflex, due to thickening and reduced elasticity of the lens. Need for reading glasses

Answer 38

``` Duration of diabetes Poor glycaemic control Hypertension Pregnancy Smoking Obesity Nephropathy ```

Answer 39

>12yrs with diabetes gets annual screening.

Answer 40

Two mechanisms: Leakage: Hyperglycaemia leads to loss of pericytes. Some exist in the capillary support system and so can lead to microaneurysm formation- early sign of diabetic retinopathy. Occlusion of capillaries: Basement membrane thickens and endothelial cells undergo apoptosis due to hyperglycaemia. This, along with loss of pericytes and increased platelet aggregation leads to occlusion and ischaemia. Retinal hypoxia upregulates VEGF.

Answer 41

Microaneurysms/leakages: Lipid exudates, oedema, haemorrhages. Occlusion of capillaries- ischaemia which can cause new vessel formation (not good as can rupture), irregular retinal veins/venous bleeding, cotton wool spots, intraretinal microvascular abnormalities (IRMA- valved branches of vessels which aim to perfuse areas of nil perfusion). IRMA are patent and do not leak whereas neovascular vessels are leaky.

Answer 42

Falls into either diabetic retinopathy: Background diabetic retinopathy Pre proliferative Proliferative (Will progress to the next stage if poor glycaemic control) or ``` Diabetic maculopathy: Focal macular oedema Diffuse macular oedema Ischaemic maculopathy Clinically significant macular oedema (CSMO) ``` All changes are seen and diagnosed when observed via a slit lamp.

Answer 43

Microaneurysm- saccular aneurysm Dot and blot haemorrhages (retinal haemorrhages) Hard exudates- lipid deposits due to leakage Cotton wool spots (ischaemia of the nerve fibre layer) Manage- Regular monitoring by an ophthalmologist.

Answer 44

Progression from BR if poor glycaemic control, leading to ischaemia. Leads to: IRMA Venous loop/bleeding Cluster of large blot haemorrhages Multiple cotton wool spots- in > 2-3 quadrants Manage by follow up in 4 months.

Answer 45

This is a more serious form of retinopathy. As a result of progression from preproliferative if poor glycaemic control and/or other vascular problems present. New vessels form either on the disc (NVD) or elsewhere (NVE). May have pre-retinal haemorrhages. Advance disease may have retinal detachment. Manage with panretinal photocoagulation treatment within 2 weeks.

Answer 46

The macula provides us with our central vision. In diabetic maculopathy, the macula sustains damage, often from diabetic macula oedema- BV next to macula leak protein/fluid. If this causes retina to harden or exudates become large next to the fovea this is termed CSMO.

Answer 47

Focal Well-circumscribed areas of leakage, with oedema. Full/partial rings of exudates often surrounding microaneurysm Treat with focal laser- takes 3 months to take effect.

Answer 48

Diffuse retinal thickness with cystoid oedema (diffuse swelling) Treat with grid laser.

Answer 49

Reduced visual acuity Normal clinical appearance Macular ischaemia on fundus fluorescent angiogram. Treat through observation

Answer 50

Retinal thickening at or within 500 microns of the centre of the macula. Hard exudates at or within 500 microns of the centre of the macula if associated with adjacent retinal thickening Retinal thickness of >1disc area, any part of which is within 1DD of the centre of the macula. Treat with Anti-VEGF

Answer 51

Combination of diffuse and ischaemic maculopathy.

Answer 52

Thickening involving the fovea centre >400 micron and visual acuity 6/9 Treatment: Anti VEGF therapies, IV Iluvien (implants) for persistent DMO which is not cured by Anti-VEGF.

Answer 53

Maculopathy is the most common cause of blindness in diabetes. T1DM is more likely to present with proliferative change. T2DM is more likely to present with maculopathy. Common complications- - Retinopathy. - Iridopathy (ischaemic changes of iris- minor iris transillumination defects). - Unstable refraction. - Orbital infection - Ocular ischaemic syndrome Less common include recurrent stye, ocular nerve palsies etc.

Answer 54

- Good glycaemic control - BP control - Reduce cholesterol - Stop smoking - Weight loss - Exercise

Answer 55

- Background: Annual screening , Systemic disease with 9-12 months hospital FU. - Pre Proliferative: 4-6/12 FU - Proliferative/Active : Pan Retinal Photocoagulation(PRP) within 2/52 - Proliferative- once stable: 4-6/12 FU - Proliferative with DMO: Macular laser to treat maculopathy first- otherwise can lose vision then PRP.

Answer 56

- Focal: Focal laser, FU 3-4/12 - Diffuse: Grid laser, FU 3-4/12 - Central involving: > 400 micron Anti VEGF - Ischaemic : observe - Persistent maculopathy: IV fluocinolone (Iluvein)

Answer 57

VH- Bleeding of normal, diseased or new BV into the vitreous humour leading to sudden onset painless vision loss. PRP same day or 2/52 later- until vision is cleared. If persistent: vitrectomy+ endolaser+ anti VEGF. R- Severe ischaemia leads to neovascularisation; where new vessels can grow over the iris- appears red and if trabecular meshwork is blocked on its course then can cause glaucoma. Urgent PRP Rubeotic glaucoma: PRP/ANTI VEGF,IOP reduction, Cyclodiode If causes VH- VITI+ Endolaser

Answer 58

``` Vision loss- corenal ulceration, glacuma, iritis Pain- amount of pain; severe- scleritis, minimal- conjunctivitis Discharge- can indicate bacterial Onset (sudden/gradual) Duration Other Symptoms? Itching? Grittiness? ```

Answer 59

- Snellen chart- Even if in A&E; need to assess VA - Ophthalmoscope (blue light to examine the anterior chamber) - Magnifying Aid - Fluorescein drops to look for corneal abrasions- will pass over normal cornea but will get 'stuck' at defects - Use slit lamps

Answer 60

Mild discomfort Purulent discharge Starts off with one eye so ask in the Hx. Good VA Manage by taking a swab and treat with chloramphenicol (ointment/eyedrops) QDS for 1 wk.

Answer 61

``` Gritty/mild discomfort Associated cold/cough Watery discharge Duration of several weeks Corneal involvement can be very painful Diffuse bilateral red eye Preauricular LN sometimes ``` Manage- Self limiting Can take a viral swab and treat with lubricants, Abx to avoid secondary bacterial infection. Steroid eye drops if cornea involved. Bilateral redness

Answer 62

Mucopurulent discharge More chronic- lasting weeks Associated STI symptoms O/E conjunctival injection, follicles (transparent collection of lymphocytes) Manage- With chlamydial swab, referral to GUM, topical Abx and systemic azithromycin/tetracycline.

Answer 63

Hx of atopy, itching and redness Diffuse injection Chemosis (swollen conjunctivae) Papillae- oedema in conjunctiva under the eyelid (cobblestone like) Manage- Topical/oral antihistamines. If severe then topical steroids.

Answer 64

Conjunctivitis of <1 month old. Gonorrhoeal/chlamydial- passed through the delivery and can result in corneal disease/blindness. Manage- Need urgent viral/bacterial/chlamydial swabs Treat with topical Abx drops, admit under paediatrics and may require systemic treatment-depending on the cause.

Answer 65

``` Localised area of inflammation of episclera Acute onset Discharge Area of irritation Sector of redness Minimal discomfort Bright red eye but no associated pain Foreign body sensation Watering eye Associated with IBD and RA ``` Usually self limiting- resolves within 7-10 days, can prescribe lubricant drops for comfort or NSAIDs. If recurrent then consider inflammatory screen.

Answer 66

``` Inflammation of the sclera. Very painful Reduced VA Photophobia Global tenderness on palpation Diffuse redness Px may wake up with it, unable to move the eye. ``` ``` Associated with: SLE RA IBD Sarcoidosis Granulomatosis with polyangiitis ``` Manage- Need immediate referral. Inflammatory screen looking for RA, Wegners, sarcoidosis etc. Treat with NSAIDs, oral prednisolone or immunosuppressants if have a systemic disease.

Answer 67

Inflammation of the cornea ``` Causes: Viral- HPV Bacterial- Staph, pseudomonas Fungal infection- Candida, aspergillus Contact lens acute red eye (CLARE) ``` Common type is Herpes simplex keratitis (HSV).

Answer 68

Bacterial Viral- Herpes Simplex Keraitis, Herpes Zoster Ophthalmicus, Adenovirus Other infections including fungal, acanthamoeba

Answer 69

``` Pain and photophobia Contact lenses Facial cold sores Rash/vesicles Recent injury/abrasions May have vision loss ``` Presents with: - Conjunctival injection - Abrasion - Hypopyon- pus in the anterior chamber - Will see on fluroscein

Answer 70

Infiltrate hypopyon. Treat intensively with hourly drops of fluroquinolones; need a few days of therapy. If more severe- use dual therapy Abx. Take samples via a corneal scrape for MCS.

Answer 71

Can occur as the first manifestation or as a recurrent. ``` Px presents with: Painful red eye Photophobia Vesicles around the eye FB sensation Watering eye Reduced VA (can be subtle or significant) A hazy cornea or cream opacity (suggests stromal keratitis) Reduced corneal sensation ``` These are dendritic ulcers due to coldsore virus. Can observe on slit lamp also take a viral swab for PCR.

Answer 72

Local anaesthetic applied with a cotton bud. Acyclovir topical/oral. Any ulceration should be treated prophylactically with chloramphenicol Abx. Any stromal keratitis may require steroid treatment. In the case of stromal keratitis, where scarring has occurred Px may require a corneal transplant.

Answer 73

These are less common corneal ulceration but more common in contact lens wears. Acanthameoba- Swimming, showering in contact lenses- water could be contaminated or sleeping in contact lenses. Trauma to the cornea creates a point of access for organisms. Manage with intensive anti-fungal/anti-amoebic drops.

Answer 74

These are partial thickness injuries of the cornea following a history of minor trauma i.e. scratch, grit, contact lenses etc. ``` Painful Watering Red Blurred vision Photophobia Foreign body sensation Hx of foreign body or contact lenses ``` ``` Causes: Contact lenses Foreign body Fingernails Eyelashes Entropian ```

Answer 75

Observe with fluorescein staining- will appear yellow, can look at more significant ones with slit lamp. Mx- Topical Abx; chloramphenicol eye drops. Lubricating eye drops. Px to return after 1 week to observe progress. Uncomplicated cases resolve within 2-3 days.

Answer 76

``` Bacterial keratitis Other types of keratitis Corneal abrasion Contact kens associated red eye (CLARE) 3 and 9 O clock staining Inferior closure stain ```

Answer 77

Chronic inflammation of eyelids. Dry eye, grittiness, redness. Can get anterior- Affecting the base of the eyelashes, either due to seborrheic keratosis or staph blepharitis caused by s.epidermidis or s.aureus. Can get posterior- Inflammation of the Meibomian glands. May also get a mixed image. Commonly associated with seborrheic dermatitis, dry eye syndrome and rosacea.

Answer 78

Good eyelid hygeine- using cotton buds to remove crustiness. Apply pressure with warm compress over Meibomian glands to express them. If these unsuccessful then use chloramphenicol Abx. Artificial tear drops for relief of symptoms, when necessary Steroid eye drops for inflammatory side, used very sparingly

Answer 79

- Red eye - Comfortable - Well demarcated subconjunctival blood - No affect on vision Check BP and clotting. Ask about coughing, weight lifting, constipation, HTN, trauma etc. Not dangerous- will resolve itself without treatment. Can give lubricating drops if foreign body sensation.

Answer 80

Fibrovascular growth of the conjunctiva. Pterygia is where the growth is over the cornea so can impair. Pingueuculum is an elevated bump/patch which does not grow over the cornea so does not need resecting. This can become inflamed and irritated, become gritty with discomfort. Surgically remove if onto the cornea, otherwise use lubricants.

Answer 81

Used to measure visual acuity. Numerator is the distance the Px is away from the chart- 6m Denominator is the distance a person with normal vision would be able to see. 6/6 or 20/20 is 'perfect vision'. E.g. VA= 6/12 ^-2 Add a -x or +x to the denominator for when the Px can't get through an entire line.

Answer 82

More standardised compared to the Snellen chart. Each line has a value of 0.1 and each letter a value of 0.02. VA= the score of the line they read + the score of the letters they can't read on the line. E.g. if a person reads to the line worth 0.6, but can only read 3/5 letters then VA= 0.6 + (2*0.02)= 0.64.

Answer 83

These are useful in children, Px with cognitive impairments or non English speakers. Examiner will look through a small pinhole in the card to objectively observe where the Px chooses to look. - Keeler Preferential Looking Cards - Cardiff Acuity Cards - Kay Pictures - LogMAR Keeler Book

Answer 84

Look towards a sheet which has group of stripes which eventually get finer. Use from age 8wks to 12months. Test 38cm away.

Answer 85

Picture located at either the top, middle of bottom of the card. Age 3-18 months, Test 50cm-1m away.

Answer 86

LogMAR- group of pictures and if Px can't articulate the answer then match with cards infront of them. 2-4yrs. Test at 3m Pictures can be crowded (objects around it) or uncrowded.

Answer 87

Letter based with matching cards. Crowded and uncrowded. 4+yrs. Test at 3m.

Answer 88

- Counting fingers - Hand movements - Perception of light- check if retina functioning. - If not responding to any then mark as No Perception of Light (NPL)

Answer 89

Cover test will differentiate between a manifest and latent deviation. Cover-uncover test shows manifest deviation: A squint present when both eyes are open, Px is alert and looking at their target. Alternate cover test shows a latent deviation: A squint most people have, slight imbalance, but when the Px is alert then can't tell. Also looking at their compensatory head posture, ptosis, nystagmus, unequal pupils etc.

Answer 90

Strabismus is the medical term for a squint. Either horizontal or vertical. Esotropia- Inward Exotropia- Outward Hypertropia- Upward Hypotropia- Downward

Answer 91

``` FHx LMBW Maternal smoking Hypertropia Downs syndrome Disease affecting nerve/muscles Premature birth Cataract Head injury ```

Answer 92

``` Eye or blood vessel damage Loss of vision Eye tumour or brain tumour Graves’ disease Stroke Various muscle and nerve disorders ```

Answer 93

TED- Commonly IR and MR affected, therefore get hypotropia and esotropia.

Answer 94

Strabismus refers to a turn in the eye- squint. | Amblyopia refers to a reduced vision, where strabismus is a common cause. (Lazy eye)

Answer 95

The visual system is immature at birth, where the fovea develops fully at 4-6 months. Up until the age of 7 yrs the visual cortex is plastic- so any correction of a strabismus should be completed before this. The axial length is shorter than that of an adult.

Answer 96

``` A unilateral (usually) reduction in visual acuity where ocular disease or obvious structural abnormality is not present. This is treatable in children. ```

Answer 97

- Strabismus - Anisometropia- difference in refractive errors between the eyes. - High bilateral refractive error - Stimulus deprivation- blockage in vision i.e. ptosis, congenital cataract etc - High Astigmatism

Answer 98

Inconcomitant is where the size and angle of squint is different in different positions of gaze, i.e. nerve palsy. Concomitant is where the angle and size of the squint is the same in different positions of gaze i.e. in children. These can be 'fully accommodative' where they are resolved by correcting the refractive error. Or they can be 'intermittent distance' where the squint changes with distance i.e. goes as move closer to stimulus. Concomitant causes include refractive error, FHx, premature, developmental delay or idiopathic.

Answer 99

Orthoptic tests- VA, CT, OM (ocular motility). Cycloplegic tests- Dilate the pupils and relax the accommodation reflex using cycloplegics to objectively assess refractive error. Eye health- Need to ensure not due to fundus or media pathology inc cataract or retinal tumour. If unusual or any red flags refer for imaging and bloods.

Answer 100

Cover test (single cover test) will detect manifest strabismus Ask pt to focus on a target Cover one eye and look at the other If there is no shift in fixation of the uncovered eye, the patient has normal alignment = orthotropic If there is a shift in fixation in the uncovered eye, then the patient has heterotropia Exotropia: the eye is outwards at rest, and moves nasally when the opposite eye is covered Esotropia: the eye is inwards at rest (nasal direction), and moves temporally when the opposite eye is covered Hypertropia: the eye is upwards at rest and moves inferiorly when the opposite eye is covered Hypotropia: the eye is downwards at rest and moves superiorly when the opposite eye is covered Cover-uncover test (alternating cover test) will detect if a latent strabismus If the above single cover test demonstrates no tropia Cover one eye for 1-2 seconds, then quickly remove the occlude to restore binocular vision The eye that was covered is observed (rather than the uncovered eye as in single cover test) for refixation movement If a phoria is present, this eye will shift back to being orthotropia to re-establish sensory fusion with the other eye Exophoria: the covered eye moves nasally when uncovered Esophoria: the covered eye moves temporally when uncovered Hyperphoria: moves inferiorly Hypophoria: moves superiorly

Answer 101

Correct the refractive error- will show results within 18-20wks. If no improvement then patch the good eye to encourage bad eye to correct itself- possible due to cortical plasticity. If still poor then surgery- although can recur it is good for confidence and prevention of long term mental health issues.

Answer 102

- Retinoblastoma: If missed can cause blindness, loss of eye, death - Congenital cataract: If missed can cause blindness To rule these out- all children are examined for red reflex at birth If dark or white- something is blocking the light, refer to Ophthalmology immediately.

Answer 103

Monocular- ghosting/shadowing of image due to uncorrected refracted error or cataracts. Usually comes from one eye. Binocular- Either horizontal or vertical diplopia depending on if the eyes are misaligned horizontally or vertically. Very debilitating and confusing for a Px. Increase risk of falling, illegal to drive. Tilt diplopia- mix of horizontal and vertical misalignment or due to torsion diplopia.

Answer 104

The visual plasticity allows for the brain to suppress parts of the retina which would accept the information that would otherwise confuse the brain and cause diplopia. Therefore children won't get diplopia, it is a symptom of adults with previously straight eyes. NB Manage diplopia with prisms.

Answer 105

CNIII has the superior and inferior branches. S- LPS, SR. I- IR, MR, IO. Partial/complete ptosis Eye depressed and abducted Dilated and unreactive pupils Oblique diplopia under the ptosis.

Answer 106

``` Microvascular- diabetes, HTN PCA aneurysm SOL Trauma Demyelinating disease GCS ```

Answer 107

Orthoptic tests- VA, CT, OM, pupils General- bloods, BP, MRI/CT, biopsy (if suspecting GCA). - Treat underlying cause, microvascular will recover at least partially 6-9 months. - Prisms to treat amblyopia in <8yrs. - Strabismus surgery just to alleviate non-recovering diplopia. Mainly improves appearance. - Can reduce residual diplopia with occlusive contact lens.

Answer 108

Posterior communicating artery aneurysm- emergency neurological referral!

Answer 109

Controls SO Prone to damage due to longer cause. -Vertical diplopia -Hypertropia -Head tilt to unaffected side usually vertical diplopia. -Torsion

Answer 110

- Back of head trauma (<45yrs usually) - Microvascular (DM, HTN) - MS - SOL - Congenital

Answer 111

Orthoptic test- VA, CT, OM, pupils General- Image if unusual i.e young but no head injury. Treat by monitoring recovery, temporary prism or surgery.

Answer 112

Lateral rectus. Susceptible to increased ICP, runs over sharp bony edge, therefore if bilateral CNVI palsy think raised ICP. - Esodeviation- larger in distance - Face turn to affected side - Horizontal diplopia- greater in distance and towards affected side - Limited abduction

Answer 113

- Raised ICP - Trauma - Infection - Microvascular - SOL - Demyelinating disease - Infection

Answer 114

Orthoptic tests- VA, CT, OM, pupils, CV (colour vision since this would be an early sign of raised ICP), PCT. General tests- BP, bloods, CT/MRI - Treat underlying cause - Monitor recovery (Microvascular disease is 6-9 months) - Prisms - Surgery to align and reduce diplopia

Answer 115

Increased ICP | Need emergency neurological imaging

Answer 116

Most microvascular palsies and childhood post-viral palsies resolve spontaneously so offer prisms or occlusion for large incomitant deviations If stable & symptomatic for >6 months, consider surgery

Answer 117

``` Congenital Problem in the development of CNVI Px unable to adduct and abduct properly Adopts a head tilt to compensate Cannot be treated Patching is irrelevant ```

Answer 118

Idiopathic autoimmune disorder, commonly associated with Graves. Two phases; Active/inflammatory- initial stage, oedema of extraocular muscles and orbital fat- pushing the eye out (proptosis). Inactive/fibrotic- changes unlikely. Affects females more than males.

Answer 119

Symptoms- - Gritty or watery eyes - Puffy eyelids - Ocular pressure or pain - Angry looking eyes - Bulging eyes - Diplopia - Visual loss - Field loss - Dyschromatopsia- colour vision problems - Depression Signs- - Proptosis- unilateral reflecting the asymmetric muscle involvement - Lid lag on downgaze (von Graefe sign) - Lid oedema - Increased IOP- glaucoma may result from decreased episcleral venous outflow, because of restrictive myopathy. - Strabismus - Optic nerve compression may occur with seemingly mild proptosis – often without visible optic nerve oedema Document visual acuity, colour vision, presence/ absence of a relative afferent pupillary defect during each visit.

Answer 120

General health Ocular health Hx- Fhx, SMOKING, occupation, hyper/hypothyroid, compliance to meds, which meds and how often they take them, symptoms, old images Examination- VA, istihara colour vision assessment, exophthalmometry, orbital tension, assess lid lag, lid retraction, corneal exposure- ulcer? Orthoptic assessment- field of binocular single vision, field of uniocular fixation, Hess chart, visual field study, take pictures TFTs, antibody screen, MRI (preferred).

Answer 121

``` Optimise endocrine control STOP SMOKING Avoid radioiodine Lubricants Ocular hypotensives Radiotherapy Surgery- orbital decompression firstly, strabismus surgery, lid surgery (upper/ lower retractions- in the fibrotic stage) ``` Clinical activity score- done when you first see them and when you see them again to see improvements/ decline. > or including 4= benefit from immunosuppression <4= risks outweigh the benefits of immunosuppression Immunosuppression options: IV or oral corticosteroids if active inflammation coexists with moderate or severe TED Pain- painful oppressive feeling on or behind globe, pain on attempted up/ down/ side gaze Redness- of eyelids or conjunctiva Swelling- of lids, chemosis, swollen caruncle, increase in proptosis of >2mm in 1-3 months Impaired function- decrease in eye movements of 5 degrees in 1-3 months, or decrease in VA on Snellens or 1 or more lines in 1-3 months

Answer 122

Autoimmune disease of NMJ, where muscles fatigue easily after movement, therefore Px feel best in the morning and worse at the end of the day. Usually presents with ocular MG before developing generalised MG.

Answer 123

- Ptosis- (variable and fatiguing between and within eyes) unilateral/bilateral. LPS very susceptible to fatigue. - Strabismus (variable) - Diplopia- changes with their strabismus - Accommodation fatigue- difficulty reading Can mimic any neve palsy, where the presentation is constantly changing.

Answer 124

Ice and rest test- Apply ice to the eye lid for 5 minutes and notice a loss of the ptosis. Orthoptic- Sustained elevation upgaze- Can't look up for more than 60 seconds. Cognas lid twitch- Eye lid twitches when looking up. Repeat examinations may show variable results. General- Diagnose with AchR antibody and electrophysiology testing.

Answer 125

Address the symptoms i.e. prisms for diplopia. Medical- Acetylcholinesterase inhibitors (pyridostigmine) combined with immunosuppressive drugs (steroids, rituximab azathioprine etc). Thymectomy may be useful. Crisis- IV IG or plasmapheresis.

Answer 126

- Unilateral proptosis - Ocular and orbital pain Causes include: - Orbital tumour; optic nerve glioma, schwannoma, sarcoma - Retrobulbar haemorrhage - Orbital pseudotumor

Answer 127

``` Temporary prisms (Fresnel prisms) Incorporated prisms ``` Occlusion; patches, occlusive contact lenses Surgery- Resection- remove part of the muscle to strengthen/tighten it. Recession- move the muscle forward to weaken it.

Answer 128

swinging tests

Answer 129

Optic nerve compromise Othe clues CAuses; optic neuritis, trauma, demyelination, galucoma, tumours, retinal abnormality,

Answer 130

TORCH nifecions can cause cataract in children. keyhole pupil- read up

Answer 131

Loss of transparency in the lens, caused by either a disruption to the configuration of lens fibres, epithelia or capsule. Leading to gradual decrease in vision affecting everyday life, glare etc. Nuclear- Affecting the nucleus of the lens- Px will become myopic. Subcapsular- Beneath the capsule- granule/plaque appearance- Px near vision will be affected. Cortical- Affecting the cortex of the lens- Px will present with astigmatism worse in the dark.

Answer 132

Common after age 40yrs. In younger Px can occur earlier if; trauma (penetration of eye or blunt trauma), eye disease (high myopia, glaucoma), systemic disease (DM, neurofibromatosis type 2), drugs (steroids). RF- FHx, steroid use, smoking, prolonged UV light exposure, increasing age, diabetes, hypocalcaemia.

Answer 133

Symptoms will be suggestive of cataracts. Ophthalmoscope will show poor red reflex. Reduced visual acuity. Ophthalmoscope will show opacity in the lens. Slit lamp confirms this and rules out any other causes.

Answer 134

Consider cataract surgery when the Px daily activities are affected i.e. driving, looking at bright lights, watching TV etc. Phacoemulsification- Most common technique in the UK. Local anaesthetic. The old lens is broken down into small pieces with ultra sound. These are then removed and replaced with a new artificial lens, which has been corrected to the Px prescription. Although the Px will have their prescription they will have still lost the accommodation reflex. Extracapsular cataract extraction- removal of the diseased nucleus and aspiration of the lens cortex, capsule left in situ and new rigid lens inserted, bigger incision required

Answer 135

Improved visual acuity Improved cloudiness Improved colour vision Most common post op complication- Posterior capsular opacification. Remaining lens epithelia will replicate so that the opaque membrane leads to decreased visual acuity, blurred vision, or glare. It occurs gradually months or years after surgery. It can be corrected by laser treatment. Also- Corneal decompensation — due to corneal oedema. Cystoid macular oedema — inflammatory fluid in the centre of the retina. Detached retina — may occur weeks or months after surgery. Dislocation of the implant lens.

Answer 136

Chronic, intermittent inflammation of the eyelid (anterior) or Meibomian glands (posterior). Usually at middle age. Burning, itching, erythema and crusting of the eyelids, worse in the mornings. Associated with acne rosacea, seborrheic dermatitis and dry eye syndrome. Clinical diagnosis, may be familial.

Answer 137

Eyelid hygiene is very important. Px should initially clean eyelids BD but can do OD when symptoms settle. Should apply warm compress on eyelids- prone to styes an chalazion. Avoid eye makeup. If ineffective; prescribe topical steroids for anterior blepharitis and oral steroids for posterior blepharitis.

Answer 138

``` Sellar mass Pituitary gland not seen separately Suprasellar extension- optic chiasm Rarely parasellar Clinically: Bitemporal hemianopia Imaging: MRI best Surgery: Trans sphenoidal ```

Answer 139

Px presents with homonymous heminaopia. Abscess- acutely unwell Metastasis- especially with a Hx of cancer

Answer 140

Changes to the macula (centre of retina) Without any pathological cause >50yrs Central vision is affected Vision is more blurred May have dark spots which get progressively bigger Straight lines appear curved/distorted Colours appear darker/less vivid than previously.

Answer 141

Drusen- collections of lipid beneath the retinal pigment epithelium (RPE) and within Bruch’s membrane Some drusen can be normal. Normal drusen are small <63 micrometres and hard. Large and greater numbers of drusen can be early sign of macular degeneration RPE abnormalities- areas of hypo/ hyperpigmentation Atrophy of RPE Degeneration of photoreceptors Neovascular (exudative) AMD- new blood vessels in choroid, easily bleed, leak, resulting in distortion & scarring of retina

Answer 142

90%- Dry ARMD Treatment involves reducing progression of disease. I.e. smoking cessation, healthy eating, visual rehabilitation, vitamins etc. 10%- Wet ARMD This is harder to treat. VEGF promotes the synthesis of new BV from the choroid to the retina. These can leak and bleed. Treat with intravitreal anti-VEGF injections.

Answer 143

- Choroid layer at the bottom, provide the blood supply to the macula - Bruch’s membrane - Retinal pigment epithelium - Photoreceptors (at the top)

Answer 144

- White/Chinese - FHx - Cardiovascular disease - Increasing age - Smoking

Answer 145

Gradual loss of central vision Reduced VA Straight lines appear more crooked/wavy Wet- Acute reduction of vision within 2-3 days. Within 2-3yrs complete vision loss. Often progresses to bilateral disease.

Answer 146

Snellen chart- reduced acuity - Scrotoma- central patch of vision loss - Amsler grid test- distortion of straight lines - Fundoscopy- Drusen - Slit lamp - Optical coherence tomography- cross-sectional views of layers of retina, to diagnose wet AMD - Fluorescein angiography- to see neovascularisation- wet AMD diagnosis if optical coherence tomography didn’t exclude it

Answer 147

``` Dry- No treatment Achieve good BP control Stop smoking Take vitamins ``` Wet- Anti-VEGF i.e. ranibizumab, bevacizumab, pegaptanib- injected directly into vitreous chamber once a month. Should see improvement within ~3 months.

Answer 148

``` HTN Diabetes Hyperlipidaemia Glaucoma >45yrs usually due to CRV thrombosis <45yrs usually due to thrombophilia Smoking Systemic disease i.e SLE ```

Answer 149

Pooling of blood in the retina Macula oedema and retinal haemorrhage Retinal tissue is damaged leading to vision loss Leads to increased release of VEGF

Answer 150

Ischaemic- - Reduced VA - RAPD - Cotton wool spots - Multiple intra-retinal bleeds - Thunder fundus Non ischaemic

Answer 151

Painless loss of vision. Fundoscopy shows; - Blot and flame haemorrhages - Macula oedema - Optic disc oedema

Answer 152

Identify any RF present and manage these. Identify any sight threatening conditions and manage these i.e. glaucoma, macular oedema, avoid neovascularisation. Photocoagulation Intravitreal steroids Anti-VEGF

Answer 153

The inner retinal surface and the optic nerve.

Answer 154

Atherosclerosis | GCA- Vasculitis causes a reduced blood flow.

Answer 155

``` Atherosclerosis- Age FHx Smoking Alcohol HTN DM Poor diet Inactivity Obesity ``` GCA- Age> 50 Females Px with GCA or PMR

Answer 156

-Sudden painless loss of vision -Relative afferent pupillary defect: Pupils of affected eye constricts more consensually (when the unaffected eye is tested) compared to direct stimulation. This is due to the ischaemic nature of the affected retina. Fundoscopy The retina has a reduced perfusion so is more paler, the macula of the retina exposes the choroid beneath-> pale retina and cherry red spots.

Answer 157

Immediate referral to Ophthalmology Giant cell arteritis- ESR, temporal artery biopsy, high dose steroids If symptoms suggest occlusion within 24 hrs, attempt to dislodge the embolus by: Firm ocular massage through closed eyelids for 15 mins Stat crushed acetazolamide 500mg PO and beta blocker Offer anterior chamber paracentesis Inhaling carbogen to dilate the artery Sublingual isosorbide dinitrate to dilate the artery Long term mx- Treating reversible risk factors Secondary prevention of CVD

Answer 158

Infarction of the optic nerve head. Arteritic cause (GCA) Non arteritic cause Sudden loss of vision

Answer 159

Male Systemic arteriopathy 40-60yrs Disc vessel crowding (disc w/o a cup, small hypermetropic discs, disc drusen)

Answer 160

- No effective treatment - Review all vascular RF & exclude GCA - Re-check clinical findings, particularly fields- expect 3 lines of VA improvement in 30% pts AION is unlikely to recur in the same eye after nerve fibre atrophy relieves disc vessel congestion. Review in 6 months, discharge if stable.

Answer 161

Separation of the inner neurosensory retina from the underlying RPE Vitreous fluid accumulates in the subretinal space The outer retina relies on the blood vessels of the choroid for blood supply

Answer 162

``` Increase age FHx Myopia Cataracts Trauma Posterior vitreous detachment Diabetic retinopathy Retinal malignancy ```

Answer 163

New floaters New flashing lights Reduction in VF, sudden onset and progressive Reduced visual acuity, blurred vision, distorted vision Curtain like shadow appearing over the vision

Answer 164

Reattach retina and reduce traction or pressure that may cause it to detach again. - Vitrectomy- removing relevant parts of vitreous body and replacing with oil or gas. More commonly used. - Scleral buckling- using a silicone buckle to put pressure on the sclera so that the outer eye indents to bring the choroid inwards and in contact with the detached retina - Pneumatic retinopexy- injecting a gas bubble into the vitreous body and positioning the pt so that the gas bubble creates pressure that flattens the retina against the choroid and close the detachment Repair retina tear- Laser therapy Cryotherapy

Answer 165

``` Stye Meibomian cyst Malignant; BCC, SCC, Bowens disease Epidermoid cysts Vascular lesion i.e. haemangioma Xanthelasma Pigmented naevi Eyelid neurofibroma ```

Answer 166

``` Although different aetiology, affect a confined space so gives rise to unspecific symptoms. Proptosis Pain Diplopia Reduced vision ```

Answer 167

1) Proptosis? 2) Progression?- Seconds (Haemorrhage), hrs-days (inflammation), wks-months (malignancy), months-yrs (benign) 3) Pain? 4) Perceptive visual change?- Colour, diplopia, blurred, refractive error change 5) Palpable mass? 6) PMH? Thyroid disease, malignancy, GCA, trauma, sinusitis 7) Periorbital abnormalities- including sensory- paraesthesia, numbness, facial weakness, redness, tenderness, watering, lid anomalies

Answer 168

``` Thyroid eye disease Orbital cellulitis Idiopathic inflammation Trauma Vascular abnormalities ```

Answer 169

Non-painful: Episcleritis Subconjunctival haemorrhage Conjunctivitis ``` Painful- Keratitis Scleritis Glaucoma Anterior uveitis Corneal abrasion/ulcer Trauma/irritant Foreign body ```

Answer 170

Turning in of the eyelids Eyelashes irritate the eyeball Causes: Involutional (aging) changes Conjunctival scarring (cicatricial) Spasm of orbicularis oculi Mx- Initially tape the eyelid down to stop eye from drying out. Regular eyedrops Eventually surgical eyelid tightening

Answer 171

Turning outward of the eyelid Causes: Aging- decreased collagen, but this is unlikely Paralytic- CNVII palsy Mechanical- lower lid heavy due to tumour or Meibomian cysts Eyelid skin scarring i.e. from eczema/previous surgery. Mx- Surgical intervention

Answer 172

Inward growth of the eyelashes, can cause corneal irritation and ulceration. Manage- Epilation- removal of eyelashes In rare cases need prevention of regrowth- laser, cryotherapy or electrolysis.

Answer 173

Destructive microbial infection of the soft tissue, causing precipitous tissue destruction, septicaemia, DIC and death. Causative organisms eg neg bacilli, strep, staph. Risk factors- advancing age, injury eg insect bite, immunosuppression including diabetes Mx- immediate IV benzylpenicillin 2.4g qds and IV clindamycin 600mg qds. Debride necrotic tissue down to a healthy (bleeding) bed. Repeat as necessary. Send tissue for culture & sensitivity. Subsequent reconstructive approaches

Answer 174

Direct injury to cornea- most often a superficial corneal abrasion Red eye, seen using fluorescein eye drops and a blue light Give chloramphenicol ointment for 5-7 days qds Exposure keratopathy Dryness of the cornea due to incomplete lid closure allowing tear evaporation & consequent failure of the tears to spread adequately across the eye surface Red eye Lid taping if there is unwanted corneal exposure Chemosis (conjunctival swelling) Risk factors- compromise venous return from ocular structures (eg from tight endotracheal tube taping), states of generalised oedema (eg fluid overload), incomplete eyelid closure can also predispose chemosis Chemosis can cause impaired eyelid closure Microbial conjunctivitis and keratitis Respiratory secretions are thought to be the major source of ocular surface infection, with aerosols from tracheal suctioning and direct contact from suction catheter both being implicated If endotracheal suctioning is done from the side of the pt (rather than at the head) and with the eyes covered, pseudomonas infection rates can be reduced Conjunctivitis: look for a red sticky eye, take swabs of the eye discharge, remove discharge by bathing eyelids with warm water, using a separate gauze for each eye. Use chloramphenicol ointment (rather than drops to aid lubrication) qds for 5-7 days Microbial keratitis: the damaged cornea is especially vulnerable to bacterial invasion which can occur rapidly. Most cases are due to bacteria & appear as a red eye, corneal ulcer. Seek urgent ophthalmology referral

Answer 175

Px unable to close their eyes? Any conjunctival exposure? Any corneal exposure? Tape eye shut- reduce dryness and protect the eye. Liberal use of eye drops/ointments- ointments last longer.

Answer 176

Vascular i.e. CRVO, CRAO, AION Retinal detachment Wet ARMD Vitreous haemorrhage

Answer 177

Dry ARMD Cataract Glaucoma

Answer 178

Common ocular malignancy in children. Average age 18 months Autosomal dominant Suspect when: Absent red reflex- appears white due to large posterior retinal tumour Strabismus Visual problems

Answer 179

Local therapy Enucleation for advanced local tumours or after treatment failure Systemic chemotherapy- multi agent chemotherapy used alone or with local treatments as primary or salvage therapy

Answer 180

Systemic HTN resulting in retinal vessel damage. | May be due to years of chronic HTN, or appear quickly after malignant HTN.

Answer 181

Stage I- Arteriolar narrowing and tortuosity Increased light reflex - silver wiring Stage II- Arteriovenous nipping Stage III- Cotton-wool exudates Flame and blot haemorrhages Stage IV- Papilloedema

Answer 182

Silver wiring or copper wiring where the walls of the arterioles become thickened & sclerosed causing increased reflection of the light Arteriovenous nipping where the arterioles cause compression of the veins where they cross, again due to sclerosis & hardening of the arterioles Cotton wool spots- due to ischaemia & infarction in the retina causing damage to nerve fibres Hard exudates- caused by damaged vessels leaking lipids into the retina Retinal haemorrhages- damaged vessels rupture & release blood into retina Papilloedema- ischaemia to the optic nerve resulting in optic nerve oedema & blurring of the disc margins

Answer 183

Control BP | Control other risk factors such as smoking and blood lipid levels

Answer 184

MS (common) Diabetes Syphilis

Answer 185

Female 30yrs Have MS Unilateral decrease in VA over hrs or days Poor discrimination of colours, ‘red desaturation’ Pain worse on eye movement Relative afferent pupillary defect Central scrotoma

Answer 186

High dose steroids Recovery usually takes 4-6 weeks Prognosis- MRI: if >3 white matter lesions, 5 year risk of developing MS is 50%

Answer 187

A systemic granulomatous disease commonest in Asian and Afro-Caribbean pts Multiple sites affected- in particular, lungs, lymph nodes, skin, liver, eyes The eyes are affected in 30-60% of cases

Answer 188

Sarcoidosis can lead to a number of ocular pathologies- mainly uveitis (bilateral) - Anterior- pain, redness, photophobia - Intermediate- inflammation of ciliary body, floaters, blurry vision - Posterior- choroiditis- may involve retinal vasculitis, floaters, visual loss Keratoconjunctivitis sicca Secondary glaucoma

Answer 189

Steroids mainly. Can use laser in the case where neovascularisation has occurred in response to ischaemia/inflammation.

Answer 190

Defined as an infection by MTB in the eye, around the eye or on its surface Not usually associated with clinical evidence of pulmonary TB Ocular manifestations of TB include scleritis, interstitial keratitis, corneal infiltrates, anterior chamber and iris nodules, anterior uveitis

Answer 191

Medical emergency Can spread intra-cranially; threat to life ``` Paranasal sinuses (most common) Oropharynx including teeth Foreign bodies Skin Trauma including iatrogenic Haematogenous spread Bacteria most common cause- strep or staph ```

Answer 192

Pre-septal cellulitis- fever, peri-ocular pain, swelling, ptosis, tenderness, redness Orbital cellulitis- similar to the above however with chemosis, conjunctival infection, reduced eye movements, +/- diplopia, vision loss, RAPD (relative afferent pupil defect), proptosis

Answer 193

Sinus disease Trauma Diabetes/immunocompromised Skin/dental infection

Answer 194

Mark area of inflamed skin to monitor improvement. Admit into hospital Monitor orbital and visual functions 2-3 times daily Give ceftriaxone IV plus flucloxacillin IV qds Consider vancomycin, clindamycin, teicoplanin or other abx for MRSA In pts >10 years old or those with chronic sinonasal disease, add metronidazole Consider IV treatment 3-5 days, provided condition improves Request CT, blood glucose, FBC, blood culture Refer sinus disease to ENT Repeat CT to exclude abscess if any deterioration occurs Urgent neurosurgical referral if there is neurological deterioration or intracranial abscess Change to oral abx when there is definite improvement Review every 2-5 days after discharge until complete resolution

Answer 195

A non-invasive diagnostic test which uses a low powered laser to scan and image the inner layers of the retina OCT can help diagnose various eye diseases- ARMD, macular oedema, glaucoma

Answer 196

Bitemporal hemianopia Central tunnel vision Typically due to optic chiasm compression by tumour (eg pituitary adenoma) Homonymous field defects Affect the same side of the visual field in each eye Commonly due to stroke, tumour, abscess Half the vision is affected Scrotoma Area of absent or reduced vision surrounded by areas of normal vision Many possible aetiologies- eg demyelinating disease (MS) and diabetic maculopathy Monocular vision loss Total vision loss in 1 eye secondary to optic nerve pathology (eg anterior ischaemic optic neuropathy) or ocular diseases (eg central retinal artery occlusion, total retinal detachment)

Answer 197

Treatment of proliferative diabetic retinopathy Treatment of diabetic macular oedema Branch and central retinal vein occlusion ARMD

Answer 198

Gold standard for treatment of many retinal diseases, such as- Neovascular AMD Diabetic macular oedema/ non proliferative or proliferative diabetic retinopathy Retinal vein occlusions Uveitis Risks- Pain/ FB sensation Bleeding- subconjunctival, vitreous haemorrhage Retinal tear/ detachment Cataract- from inadvertently hitting the lens Infection- endophthalmitis Uveitis

Answer 199

Characterised by persistent or recurrent complex hallucinations (usually visual or auditory), occurring in clear consciousness Generally this is against a background of visual impairment Insight is usually preserved Risk factors- advanced age, peripheral visual impairment, social isolation, sensory deprivation, early cognitive impairment

Answer 200

7.3-7.6 Any chemical damage to the eye needs immediate topical LA and irrigating for 30 mins at least with saline. Ensure to remove any contact lenses. Continue irrigating until a normal pH is achieved. NB- can take up to 20L saline to irrigate an eye back to normal pH. Further management may require broad spectrum topical Abx, cycloplegics, therapies to encourage re epithelisation i.e. tear substitution, citric acid etc. Steroids used cautiously. After 1-2 days review for ischaemia, debride any necrotic tissue and use preservative free drops. May require surgery.

Answer 201

Lids- burned/oedematous | Conjunctiva- chemosis, epithelial loss, haemorrhage

Answer 202

Acid- When in contact with the eye will lead to the production of tissue protein, thus producing a barrier against any further chemical damage. Alkali- Is lipophilic so will penetrate the eye faster, into the ant chamber and can damage the ciliary body. Will not produce a protective protein layer, can lead to corneal damage through pH change, ulceration and collagen synthesis defects. Alkali injury is much worse than acid.

Answer 203

- Red except for pallor vessels close to the limbus. - Cloudy cornea - Hazy view of the iris Chemical injury leads to damaged pluripotent limbal stem cells. This causes corneal opacification, neovascularisation and extensive scarring. Severe burn may cause ischaemia to the conjunctival BV therefore conjunctival injection may not appear as intense.

Answer 204

``` Corneal scarring Poor vision Dry eyes Glaucoma Uveitis Cataract ```

Answer 205

``` Diplopia on upward gaze Derangement of globe position Intercanthal distance increased Oculovagal symptoms- bradycardia, hypotension, N&V) Visual disturbance Peri-orbital ecchymosis (bruising) Peri-orbital oedema Nerve sensory loss- numbness over cheek, lower eyelid, upper lip and upper teeth and gums on affected side ```

Answer 206

Time, distance and trajectory of assault/foreign body. The foreign body, has it all been recovered? Any other ocular symptoms? Any ENT symptoms i.e. epistaxis, CSF rhinorrhoea?

Answer 207

Corneal scarring

Ophthalmology Flashcards

(231 cards)