Ophthalmology Flashcards

Question

what are the ocular manifestations of RA?

Answer 1

keratoconjunctivitis sicca (most common) episcleritis (erythema) scleritis (erythema and pain) corneal ulceration keratitis Iatrogenic steroid-induced cataracts chloroquine retinopathy

Answer 2

miosis (small pupil) ptosis enophthalmos* (sunken eye) anhidrosis (loss of sweating one side)

Answer 3

Central lesions (anhidrosis of the face, arm and trunk) - Stroke Syringomyelia Multiple sclerosis Tumour Encephalitis Pre-ganglionic lesions (anhidrosis of the face) Pancoast's tumour Thyroidectomy Trauma Cervical rib Post-ganglionic lesion (no anhidrosis) Carotid artery dissection Carotid aneurysm Cavernous sinus thrombosis Cluster headache Congental horners - they will have heterchromia (difference in iris colour)

Answer 4

apraclonidine drops (an alpha-adrenergic agonist) can be used: causes pupillary dilation in Horner's syndrome due to denervation supersensitivity but produces mild pupillary constriction in the normal pupil by down-regulating the norepinephrine release at the synaptic cleft

Answer 5

multiple sclerosis: the commonest associated disease diabetes syphilis

Answer 6

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

Answer 7

Investigation MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases Management high-dose steroids recovery usually takes 4-6 weeks

Answer 8

commonly seen in woman it is one of the differential of a 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 absent ankle/knee reflexes

Answer 9

sudden painless loss of vusuin characterised by a dense shadow starting peripherally and processing centrally

Answer 10

ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery vitreous haemorrhage retinal detachment retinal migraine

Answer 11

due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve

Answer 12

incidence increases with age, more common than arterial occlusion causes: glaucoma, polycythaemia, hypertension severe retinal haemorrhages are usually seen on fundoscopy

Answer 13

due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis) features include afferent pupillary defect, 'cherry red' spot on a pale retina

Answer 14

causes: diabetes, bleeding disorders, anticoagulants features may include sudden visual loss, dark spots

Answer 15

Posterior vitreous detachment Flashes of light (photopsia) - in the peripheral field of vision Floaters, often on the temporal side of the central vision Retinal detachment Dense shadow that starts peripherally progresses towards the central vision A veil or curtain over the field of vision Straight lines appear curved Central visual loss Vitreous haemorrhage Large bleeds cause sudden visual loss Moderate bleeds may be described as numerous dark spots Small bleeds may cause floaters

Answer 16

Posterior vitreous detachment is the 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, as they may result in permanent loss of vision.

Answer 17

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 an increased risk of ischaemic cardiovascular disease, such as hypertension, dyslipidaemia and diabetes mellitus.

Answer 18

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 known 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 the 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)

Answer 19

subacute onset of visual loss with: a reduction in visual acuity, particularly for near field objects gradual in dry ARMD subacute in wet ARMD 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 visual hallucinations may also occur resulting in Charles-Bonnet syndrome

Answer 20

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.

Answer 21

slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time. fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation. optical coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren't visible using microscopy alone.

Answer 22

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. laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.

Answer 23

Keith-Wagener classification of hypertensive retinopathy I - Arteriolar narrowing and tortuosity Increased light reflex - silver wiring II - Arteriovenous nipping III - Cotton-wool exudates Flame and blot haemorrhages These may collect around the fovea resulting in a 'macular star' IV- fsclePapilloedema

Answer 24

Horner's syndrome - anhydrosis determines site of lesion: head, arm, trunk = central lesion: stroke, syringomyelia just face = pre-ganglionic lesion: Pancoast's, cervical rib absent = post-ganglionic lesion: carotid artery

Answer 25

acute onset pain blurred vision and photophobia small, fixed oval pupil, ciliary flush

Answer 26

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

Answer 27

Acquired causes multiple sclerosis papilloedema (longstanding) raised intraocular pressure (e.g. glaucoma, tumour) retinal damage (e.g. choroiditis, retinitis pigmentosa) ischaemia toxins: tobacco amblyopia, quinine, methanol, arsenic, lead nutritional: vitamin B1, B2, B6 and B12 deficiency Congenital causes Friedreich's ataxia mitochondrial disorders e.g. Leber's optic atrophy DIDMOAD - the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome)

Answer 28

Keratitis describes inflammation of the cornea. Microbial keratitis is not like conjunctivitis - it is potentially sight threatening and should therefore be urgently evaluated and treated.

Answer 29

bacterial - staph aureus or pseudomonas aerguinosa in contact lens wearers fungal amoebic - acanthamoebic keratitis, accounts for around 5% of cases, increased incidence if eye exposure to soil or contaminated water, pain is classically out of proportion to the findings parasitic: onchocercal keratitis ('river blindness')

Answer 30

red eye: pain and erythema photophobia foreign body, gritty sensation hypopyon may be seen

Answer 31

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

Answer 32

corneal scarring perforation endophthalmitis visual loss

Answer 33

dilation of the pupil

Answer 34

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

Answer 35

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 Paton's lines: concentric/radial retinal lines cascading from the optic disc

Answer 36

space-occupying lesion: neoplastic, vascular malignant hypertension idiopathic intracranial hypertension hydrocephalus hypercapnia Rare causes include hypoparathyroidism and hypocalcaemia vitamin A toxicity

Answer 37

Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer. Features red, painful eye photophobia epiphora visual acuity may be decreased fluorescein staining may show an epithelial ulcer

Answer 38

management immediate referral to an ophthalmologist topical aciclovir

Answer 39

Dacryocystitis is infection of the lacrimal sac Features watering eye (epiphora) swelling and erythema at the inner canthus of the eye Management is with systemic antibiotics. Intravenous antibiotics are indicated if there is associated periorbital cellulitis

Answer 40

Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia

Answer 41

non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy

Answer 42

Mild NPDR 1 or more microaneurysm Moderate NPDR microaneurysms blot haemorrhages hard exudates cotton wool spots ('soft exudates' - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR Severe NPDR blot haemorrhages and microaneurysms in 4 quadrants venous beading in at least 2 quadrants IRMA in at least 1 quadrant

Answer 43

retinal neovascularisation - may lead to vitrous haemorrhage fibrous tissue forming anterior to retinal disc more common in Type I DM, 50% blind in 5 years

Answer 44

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

Answer 45

if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors

Answer 46

regular observation if severe/very severe consider panretinal laser photocoagulation

Answer 47

panretinal laser photocoagulation following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue other complications include a decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina), a generalised decrease in visual acuity and macular oedema intravitreal VEGF inhibitors often now used in combination with panretinal laser photocoagulation examples include ranibizumab strong evidence base suggests they both slow progression of proliferative diabetic retinopathy and improve visual acuity if severe or vitreous haemorrhage: vitreoretinal surgery