Opthalmology Flashcards
What are the causes of sudden visual loss?
Vitreous haemorrhage Retinal artery occlusion Retinal vein occlusion Haemorrhagic wet age related macular degeneration Ischaemic optic neuropathy Pituitary apoplexy CVD Trauma
(retinal detachment and optic neuritis cause rapid but not sudden loss of vision)
How would you describe a persons eye position?
Conjugate or dysconjugate
What are the symptoms and causes of vitreous haemorhage?
Blurred vision, floaters, flashes, sudden visual loss
Reduced red reflex
Dense haemorrhage can completely obscur the retina
Retinal neovascularisation
What are the stages of diabetic retinopathy?
Non-proliferative diabetic retinopathy
- Mild: at least one microaneurysm
- Moderate: haemorrhages, microaneurysm and hard exudates
- Severe (4-2-1): microaneurysms & haemorrhages in all 4 quadrants, venous beading in 2 quadrants, microvascular abnormalities in 1 quadrant
Proliferative diabetic retinopathy
- Neovascularisation
- Preretinal & vitreous haemorrhage
What signs do you get in maculopathy?
Central visual loss
Focal or diffuse macular oedema
Hard exudates and thickening
Siginificant when found close to fovea
Describe the pathophysiology of diabetic retinopathy?
Microangiopathy that results in
a) vascular occlusion
b) leakage of plasma constituents outside of vessels
Vascular occlusion results in retinal ischaemia which leads to angiogenic factors (VEGF) that drive growth of new vessels
How would you manage diabetic retinopathy/maculopathy?
Primary prevention
- Glycaemic control (sudden intensive control can worsen it)
- BP control
- Lipid control
- Smoking cessation
- Diet
Laser therapy- aims to induce regression of new blood vessels and reduce macular thickening
Macular oedema is treated 1st by focal laser burns
Diabetic retinopathy by pan-retinal photocoagulation
Intravitreal steroids used in macular oedema
anti- VEGF- macular oedema
What symptoms would you get with retinitis pigmentosa?
Initially difficulty with night vision and gradual loss of peripheral vision
Age at presentation usually 10-30yrs
Most people retain a central tunnel vision
Name some causes of gradual visual loss?
Cataract Age related macular degeneration Diabetic maculopathy Glaucoma Retinitis pigmentosa Optic atrophy- compressive, toxic, nutritional
How is retinitis pigmentosa inherited?
Can be AD, AR, sex linked recessive, mitochondrial
50% sporadic in UK (no FH likely recessive)
15-20% likely dominant
What syndromes are assoc with RP?
Usher syndrome
Refsum disease
Lawrence- Moon-Bardet-Beidl syndrome
Kearns - Sayre syndrome
What are features of Usher syndrome?
Congenital neurosensory deafness
Retinitis pigmentosa
What are the features of Refsum disease?
Deafness Cerebellar ataxia Peripheral neuropathy Cardiomyopathy Icthyosis Palpable peripheral nerves Retinitis pigmentosa
What are features of Lawrence- Moon- Bardet- Biedl syndrome?
Deafness Polydactyly (extra fingers/toes) Short stature LD Hypogonadism Renal disease Diabetes Retinitis pigmentosa
What are the features of Kearns- Sayre syndrome?
Chronic progressive external opthalmoplegia
Cardiac conduction defects
Retinitis pigmentosa
Inherited as mitochondrial trait
What investigations would you want to do for somebody with retinitis pigmentosa?
Automated/Goldman perimetry Electrophysiology (determine retinal damage) Audiology Phytanic acid levels (Refsum disease) Molecular genetic levels
Name some causes of optic atrophy
Hereditary
- slowly progressive dominant trait
- rapidly progressive- Lebers optic atrophy
- part of syndrome DIDMOAD
Compressive
- optic nerve glioma/meningioma
- Intra-orbital eg thyroid eye disease
- Inflammatory mass eg sarcoid
- lesion of anterior cranial fossa eg frontal meningioma
- Pit tumour/craniopharyngioma
Ischaemic:
- arteritic: GCA
- non-arteritic
Demyelination
- MS
- neuromyelitis optica
Inflammatory
- Non-infective
- infective: TB, syphilis, Lyme disease
Nutritional/ Toxic
- B12 def
- Tobacco, drugs
Trauma
How would you grade thyroid eye disease?
NO- SPECS
0: No signs or symptoms
1: Only signs (lid retraction, stare +/- lid lag)
2: Soft tissue involvement
3: Proptosis
4: Extraocular muscle involvement
5: Corneal involvement
6: Sight loss (optic nerve involvement)
How would you manage a patient with thyroid eye disease?
Active acute disease:
- tear film lubrication
- steroids or other steroid sparing agent
- STOP SMOKING
- optimise thyroid control
Optic nerve compression (emergency)
- Systemic immunosuppression
- surgical decompression of orbital apex
- Orbital radiotherapy
Corneal exposure
- Tear film lubrication
- systemic immunosuppression
- surgical decompression of orbit or lid lengthening surgery
Burn out disease- burns out over 1-5yrs and once stable surgery is often performed to improve appearance and minimise diplopia
What would be important to ask about in the history of somebody with a bitemporal hemianopia?
Local pressure effects- headache, double vision
Symptoms of hypopituitarism
- hypothyroidism
- amenorrhoea, libido, erectile dysfunction
- tiredness, depression, abdo pain
Symptoms of acromegaly
Prolactinoma
What are the differential diagnoses for a bitemporal hemianopia?
Chiasmal compression
- From below: pituitary adenoma/apoplexy
- From above: craniopharyngioma
- Other: meningioma, ICA aneurysm
Non chiasmal
- nasal retinitis pigmentosa,
- Tilted optic discs
How would you investigate somebody presenting with a bitemporal hemianopia?
MRI pit
Hormonal level measurement: prolactic, IGF-1, ACTH, cortisol, TFT, FSH/LH, testosterone, short synacthen test, GGT, water deprivation test
Manage- transphenoidal surgery except prolactinoma (dopamine agonists)
Why would a homonymous hemianopia show macular sparing?
Macular visual cortex receives its blood supply from terminal branches of posterior and middle cerebral arteries, the posterior artery supplies remaining visual cortex. Hence in posterior cerebral artery obstruction the MCA spares the ipsilateral macular visual cortex
Highly suggestive of an occipital lobe lesion
What are the differential diagnoses of a homonymous hemianopia?
Infarction
- Disease in artery: atheroma, vasculitis, thrombus
- Embolic disease: AF, valve disease, carotid stenosis or vertebral stenosis
Haemorrhage
Mass lesion- tumour
Demyelination- MS
Other: migraine, trauma
Can the patient drive with a homonymous hemianopia?
No, contact DVLA and they will assess ability to drive
What are the possible causes of 3rd nerve palsy?
Solitary and pupil sparing: diabetes
Compressive: Posterior communicating artery aneurysm, ICA aneurysm, meningioma, parasellar tumour
Brainstem infarction: Webers(contralateral hemiparesis) and Benedicts (contralateral ataxia)
REMEMBER BRIEFLY assess power/tone in arms and legs
Brainstem demyelination: MS
Other: GCA. trauma, congenital
What is your investigation plan and management of somebody with a 3rd nerve palsy?
Need to find out if compressive as would need much more urgent treatment
- compressive/complex- urgent MRI/MRA/CT angio and if aneurysm then urgent neurosurgical referral
- if solitary, pupil sparing: check BP, glucose, lipids, review risk factors. If no CV risk factors perform MRI to exclude compressive
What is important in a history of somebody with Horners syndrome?
History of malignancy
Pain: headache, neck pain, arm pain
Neck trauma or surgery
Other neurological inovlement
Describe the order of the sympathetic innervation to the eye?
3-neuron arc
1st order: originates in hypothalamus and descends through brainstem to cervical cord at level of T1/2
2nd order- preganglionic: projects from spinal cord to superior cervical ganglion
3rd order neuron- post ganglionic: via internal carotid artery to orbit and innervates dilator muscles of iris
What are the causes of horners syndrome?
1st order neurons:
- Brainstem: stroke, tumour, demyelination
- Spinal cord: syringomyelia, tumour, trauma
2nd order neurons:
- lung apex: pancoasts tumour
- neck: cervcal nodes, surgery, trauma, common carotid artery dissection
3rd order:
Internal carotid artery: dissection
Cavernous sinus: thrombosis/tumour
Orbit: tumour
How would you investigate Horners syndrome?
Determine site of lesion
- hydroxyamphetamine 1% causes stimulated release of stored noradrenaline from post ganglionic neuron, if intact the pupil will dilate (1st or 2nd order)
1st order: MRI brain/spine
2nd order: CXR, CT thorax, LN biopsy, MRI, carotid Doppler
3rd order: MRI/MRA head and neck, carotid Doppler, MRI cavernous sinus
What is glaucoma?
Glaucoma refers to a group of eye conditions that lead to damage to the optic nerve head with progressive loss of retinal ganglion cells and their axons. This leads to a progressive loss of visual field
Usually assoc with raised intraocular pressure
What is open and closed angle glaucoma and how might they present?
Open angle: less severe, asymptomatic, reduction visual fields, later acuity reduced
(increased cup to disc ratio)
Closed angle- pain, blurred vision, halos
How do you manage glaucoma?
Beta blockers: timolol
Carbonic anyhydrase inhibitors: acetazolamide
Sympathomimetics
Miotics
Surgery: iridotomy, trabeculectomy
