Opthalmology Flashcards
Pathophysiology of acute angle closure glaucoma?
IOP secondary to an impairment of aqueous outflow
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age
Features of acute angle closure glaucoma?
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
Management of acvute angle glaucoma?
Combination of eye drops, for example:
1.Direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
2. Beta-blocker (e.g. timolol, decreases aqueous humour production)
3. Alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)
Plus:
Intravenous Azetazolamide
WHat is definitive management of acute angle closure glaucoma?
laser peripheral iridotomy
creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle
Most common cause of blindness in the UK?
Age related malcula degenration
Risk factors of age regulated macular degeneration?
Age
Smoke
Family history
What are the two forms of age related macular degeneration
Dry form - characterised by drusen - yellow round spots in Bruch’s membrane
Wet form - exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
Presentation of ARMD?
reduction in visual acuity, particularly for near field object
difficulties in dark adaptation - poor night vision
fluctuations in visual disturbance
suffer from photopsia, (a perception of flickering or flashing lights)
distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen
wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
Investigation of choice for ARMD?
Initial: slit-lamp microscopy is the initial investigation of choice
If postivie: fluorescein angiography is utilised if neovascular ARMD is suspected - guides anti VEGF
ocular coherence tomography is used to visualise the retina in three dimensions
What guides anti- VEGF in ARMD?
fluorescein angiography
Management of dry ARMD?
combination of zinc with anti-oxidant vitamins A,C and E
Management of wet ARMD?
anti-VEGF agents can limit progression of wet ARMD
anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,.
What are angiod retinal streaks?
irregular dark red streaks radiating from the optic nerve head.
Causes of angiod retinal streaks?
pseudoxanthoma elasticum
Ehler-Danlos syndrome
Paget’s disease
sickle-cell anaemia
acromegaly
HLA association with anterior uvetitis?
HLA B27
Factures of anterior uveitis?
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 conditiosn of anterior uveitis?
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen
Management of anterior uveitis?
- urgent review by ophthalmology
- cycloplegics (dilates the pupil which helps to relieve 3. pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
What is an argle robertson pupile?
Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
small, irregular pupils
no response to light but there is a response to accommodate
Risk factors of argyle robertson pupil?
Diabetes
Syphilus
Pathophysiology in blepharitis?
meibomian gland dysfunction (common, posterior blepharitis)
seborrhoeic dermatitis/staphylococcal infection
Features of 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 of belpharitis?
Hot compresses
Features of central retinal artery occlusion?
sudden, painless unilateral visual loss
relative afferent pupillary defect
‘cherry red’ spot on a pale retina
Either from thromboembolism or arteritis - temporal arteritis
Risk factors for central retinal vein occlusion?
increasing age
hypertension
cardiovascular disease
glaucoma
polycythaemia
Features of central retinal vein occlusion@?
sudden, painless reduction or loss of visual acuity, usually unilaterally
fundoscopy
widespread hyperaemia
severe retinal haemorrhages - ‘stormy sunset’
Management of central retinal vein occlusion
the majority of patients are managed conservatively
indications for treatment in patients with CRVO include:
macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
retinal neovascularization - laser photocoagulation
Pathophysiology of diabetic retinopathy?
Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls.
Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy.
formation of microaneurysms.
Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia
Features of mild diabetic retinopathy?
(non-proliferative)
1 or more microaneurysm
Features of moderate diabetic retinopathy?
(non-proliferative)
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
Features of severe diabetic retinopathy?
(Non-proliferative)
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Features of proliferative diabetic retinopathy?
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
Treatment of maculopathy in diabetic retinopathy?
intravitreal vascular endothelial growth factor (VEGF) inhibitors
Management of proliferative diabetic retinopathy?
panretinal laser photocoagulation
intravitreal VEGF inhibitors
ranibizumab
severe or vitreous haemorrhage: vitreoretinal surgery
Most common cause of corneal dendritic ulcer?
Herpes simplex
Features of herpes simplex keratitis?
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer
Features of herpes simplex keratitis?
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer
Management of herpes simplex keratitis?
immediate referral to an ophthalmologist
topical aciclovir
WHat is herpes zoster ophthalmicus?
Reactivation of herpez zoster in ophthalmic division of trigeminal nerve
Features of herpes zoster ophthalmicus?
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 of herpes zoster opthalmicus?
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
topical antiviral treatment is not given in HZO
topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review
Complications of herpes zoster ophthalmicus?
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia
What is Holmes addie pupil?
benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.
Feautres of holms addie pupil
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
What is holms addie syndrome?
association of Holmes-Adie pupil with absent ankle/knee reflexes