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
Features of horner’s syndrome?
miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)
Horners + Heterochromia?
congenital Horner’s
What are the three areas a lesion may be to cause horners?
Central
Preganglionic
Post ganglionic
Features of central hroners and causes?
Anhidrosis of face, arms trunk
Stroke
Syringomyelia
Multiple sclerosis
Features of preganglionic lesion horners/
Anhidrosis of face
Pancoast’s tumour
Thyroidectomy
Trauma
Cervical rib
Features of post ganglionic lesions horners?
Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache
Features of grade 1 hypertensive retinopathy?
Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
Features of grade 2 hypertensive retinopathy?
Arteriovenous nipping
Features of grade 3 hypertensive retinopathy?
Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’
Features of grade 4 hypertensive retinopathy?
Papilloedema
What is keratitis?
Inflammation of cornea - sight ending possibly
red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen
Causes of keratitis?
Bacterial
- typically Staphylococcus aureus
- Pseudomonas aeruginosa is seen in contact lens wearers
Fungal
- amoebic
- acanthamoebic keratitis
parasitic: onchocercal keratitis (‘river blindness’)
Management of keratitis?
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
What is dacrocystitis?
infection of the lacrimal sac
watering eye (epiphora)
swelling and erythema at the inner canthus of the eye
Causes of mydriasis ( dilated) eye?
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
Causes of optic atrophy?
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
Causes of congenital optic atrophy?
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)
Causes of optic neuritis?
multiple sclerosis: the commonest associated disease
diabetes
syphilis
Features of optic neuritis?
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
Best investigation of optic nueirits?
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
Management of optic neuritis?
high-dose steroids
recovery usually takes 4-6 weeks
Management of optic neuritis?
high-dose steroids
recovery usually takes 4-6 weeks
What is orbital cellulitis?
infection affecting the fat and muscles posterior to the orbital septum,
Presentation of orbital cellulitls?
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)
Most common bacteria for orbital cellulitis?
Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
Papilloedema findings on 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
Paton’s lines: concentric/radial retinal lines cascading from the optic disc
Causes of papilloedema?
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
Rare causes of papilloedema?
hypoparathyroidism and hypocalcaemia
vitamin A toxicity
Feautres of posterior vitreal 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)
Finds of posterior vitreal detachment on fundoscopy?
Weiss ring on ophthalmoscopy
Management of posterior vitreal detachment?
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.
Mechanism of prostaglandin analogues in glaucoma?
Increases uveoscleral outflow
Mechanism of beta blockers in glaucoma?
Reduces aqueous production
Mechanism of Sympathomimetics n glaucoma?
brimonidine, an alpha2-adrenoceptor agonist)
Reduces aqueous production and increases outflow
Mechanism of carbonic anhydrase inhibitors?
Dorzolamide
Reduces aqueous production
Mechanism of miotics in glaucoma?
Increases uveoscleral outflow
Red eye + small fixed pupil?
acute angle closure
severe pain (may be ocular or headache)
decreased visual acuity, patient sees haloes
semi-dilated pupil
hazy cornea
Red eye + small, fixed oval pupil, ciliary flush?
Anterior uveitis
acute onset
pain
blurred vision and photophobia
small, fixed oval pupil, ciliary flush
Scleritis?
severe pain (may be worse on movement) and tenderness
may be underlying autoimmune disease e.g. rheumatoid arthritis
Endopthalmoous
Endophthalmitis
typically red eye, pain and visual loss following intraocular surgery
What is marcus gunn pupil?
Relative afferent pupillary defect
Features of relative afferent pupillary defect?
the affected and normal eye appears to dilate when light is shone on the affected
Causes of relative afferent pupillary defectr?
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis
Pathway of pupillary light reflex?
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
Features of retinitis pigmentosa?
night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Associated diseases of retinitis pigmentosa?
Kearns-Sayre syndrome
Alport’s syndrome
Ocular manifestations of rheumatoid arthritis?
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
What visual problem does chloroquine cause?
Retinopathy
What visual problem do steroids cause?
Cataracts
Management of amarouosis fugax?
Asprin 300 mg
Fundoscopy of central retinal vein occlusion?
severe retinal haemorrhages are usually seen on fundoscopy
Fundoscopy of central retinal artery occlusion?
features include afferent pupillary defect, ‘cherry red’ spot on a pale retina
Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision
Posterior vitreal detachment
Dense shadow that starts peripherally progresses towards the central vision
Retinal detachment
Tunnel vision causes?
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
Anhidrosis horners?
head, arm, trunk = central lesion: stroke, syringomyelia
just face = pre-ganglionic lesion: Pancoast’s, cervical rib
absent = post-ganglionic lesion: carotid artery
Episcleritis painful?
No
Associated with RA
Macular degenration biggest risk facotr?
smoking
Central retinal vein loss, painful?
No
What are the major risks for orbital cellulitis?
Cavernous sinus thrombosis
Intracranial spread
First line drop in glaucoma for asthmatics?
Prostaglandins
black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Retinitis pigmentosa
What is a postive relative afferent pupillary defect?
relative afferent pupillary defect is when the affected and normal eye appears to dilate when light is shone on the affected eye
Durgs that increase acute angle closure glaucoma?
Anti muscarinics
TCI’s
Treatment of herpes zoster ophtalmicus?
Oral aciclovir
Enlarging dark spot
Vitreous haemorrhage
Dense shadow
Retinal detachment
