TO DO OPHTHALMOLOGY Flashcards
(142 cards)
1
Q
OPEN-ANGLE GLAUCOMA
what are the risk factors?
A
increased age
family history
black
myopia (nearsighted)
hypertension + CVD
diabetes mellitus
corticosteroid use
2
Q
OPEN-ANGLE GLAUCOMA
what is the clinical presentation?
A
often presents insidiously + detected during routine eye exams
SYMPTOMS
- asymptomatic
- peripheral vision loss (progressive)
SIGNS
- raised intraocular pressure
- visual field defect (peripheral loss, leading to tunnel vision)
- decreased visual acuity
- open iridocorneal angle
- fundoscopic findings (optic disc cupping, bayonetting of vessels, cup notching, optic disc haemorrhages and disc haemorrhages)
3
Q
OPEN-ANGLE GLAUCOMA
what are the investigations?
A
- standard automated perimetry (for visual field assessment)
- goldmann applanation tonometry (for intraocular pressure measurement)
- slit lamp (assess optic nerve health)
- gonioscopy (assess peripheral anterior chamber)
- central corneal thickness assessment
4
Q
OPEN-ANGLE GLAUCOMA
what is the management?
A
1st line
- topical prostaglandin analogue (LATANOPROST) or prostamide (BIMATOPROST)
- topical beta-blocker (TIMOLOL)
2nd line
- switch to drug in other 1st line drug class
- combine topical prostaglandin analogue/prostamide with topical beta-blocker
- switch to/add in one of following drugs:
= topical sympathomimetic (BRIMONIDINE TARTRATE)
= topical carbonic anhydrase inihibitor (BRINZOLAMIDE)
= topical miotic (PILOCARPINE HYDROCHLORIDE)
refractory cases
- laser (selective laser trabeculoplasty)
- surgery (trabeculectomy)
5
Q
GLAUCOMA MEDICATIONS
what are the side effects of prostaglandin analogue drops (e.g. latanoprost)?
A
- eyelash growth
- eyelid pigmentation
- iris pigmentation (browning)
6
Q
ACUTE ANGLE CLOSURE GLAUCOMA
which medications can precipitate it?
A
- Adrenergic medications (e.g., noradrenaline)
- Anticholinergic medications (e.g., oxybutynin and solifenacin)
- Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
7
Q
ACUTE ANGLE CLOSURE GLAUCOMA
what is the clinical presentation?
A
SYMPTOMS
- unilateral red, painful eye
- pain worse in the dark
- blurred vision
- haloes around lights
- headache (may be severe)
- nausea and vomiting
SIGNS
- hard, red eye
- fixed, dilated pupil
- corneal oedema (dull, hazy cornea)
- reduced visual acuity
8
Q
ACUTE ANGLE CLOSURE GLAUCOMA?
what is the initial management?
A
- lie patient flat
- analgesia + antiemetics
following may be given in combination:
- 1st line = carbonic anhydrase inhibitor (ACETAZOLAMIDE)
- topical beta-blocker (TIMOLOL)
- topical alpha-2-agonist (BRIMONIDINE)
- topical cholinergic (PILOCARPINE)
DEFINITIVE TREATMENT
- iridotomy
9
Q
GLAUCOMA MEDICATIONS
how does miotics (e.g. pilocarpine) work?
A
- Pupil constriction
- pulls iris away from trabecular meshwork increasing drainage of aqueous humour
10
Q
GLAUCOMA MEDICATIONS
how does carbonic anhydrase inhibitors (e.g. acetazolamide) work?
A
decreases the production of aqueous humour.
11
Q
ACUTE ANGLE CLOSURE GLAUCOMA
what is the definitive treatment?
A
Laser iridotomy
This involves making a hole in the iris using a laser, which allows the aqueous humour to flow directly from the posterior chamber to the anterior chamber.
12
Q
AGE RELATED MACULAR DEGENERATION
what are the risk factors?
A
- increasing age
- smoking (doubles risk of developing ARMD)
- family history
- cardiovascular disease
- obesity
- poor diet (low in vitamin and high in fat)
13
Q
AGE RELATED MACULAR DEGENERATION
what is dry age related macular degeneration?
A
also known as atrophic
is 85-90% of cases
characterised by drusen
progresses slowly over decades
14
Q
AGE RELATED MACULAR DEGENERATION
what is wet age related macular degeneration?
A
10-15% of cases
also known as exudative or neovascular
characterised by choroidal neovascularisation
leakage of serous fluid and blood result in rapid loss of vision
has worse prognosis
15
Q
AGE RELATED MACULAR DEGENERATION
what is the clinical presentation?
A
Visual changes associated with AMD tend to be unilateral, with:
- Gradual loss of central vision
- Reduced visual acuity
- Crooked or wavy appearance to straight lines (metamorphopsia)
- poor vision at night
- photopsia (perceived flickering of lights)
- gradually worsening ability to read small text.
SIGNS
- visual distortion (particularly line perception- metamorphopsia)
- drusen (yellow spots) in dry ARMD
- subretinal/intraretinal haemorrhages in wet ARMD
16
Q
AGE RELATED MACULAR DEGENERATION
what are the investigations?
A
- slit lamp = identification of exudative, pigmentary or haemorrhagic changes in retina
- colour fundus photography = monitor progression
- Fluorescein angiography = to identify neovascular ARMD + guide anti-VEGF therapy
- OCT scan = assess all layers of retina + identification of disease not visible by slit lamp
17
Q
ANTERIOR UVEITIS
what is it associated with?
A
HLA-B27
Seronegative spondyloarthropathies (e.g., ankylosing spondylitis, psoriatic arthritis and reactive arthritis)
Inflammatory bowel disease
Sarcoidosis
Behçet’s disease
18
Q
ANTERIOR UVEITIS
what is the clinical presentation?
A
SYMPTOMS
- painful, red eye
- photophobia
- tear formation
- blurred vision, then a reduction in visual acuity
SIGNS
- red eye
- presence of hypopyon (pus cells in anterior chamber which can show fluid level)
- presence of keratic precipitates
- ciliary flush (dilated ciliary vessels spreading outwards from pupil)
- small or irregular pupil
19
Q
ANTERIOR UVEITIS
what are the investigations?
A
- physical exam (visual fields, acuity, CN assessment)
- slit lamp
to consider
- infection/autoimmune screen
20
Q
ANTERIOR UVEITIS
what is the management?
A
urgently refer to ophthalmologist for review within 24hrs
1st line
- corticosteroids (topical, orally, IV, or ocular injections)
- cycloplegic-mydriatic drug (CYCLOPENTOLATE 1% or ATROPINE 1%)
- antimicrobials
2nd line
- immunosuppressants (DMARDS)
- surgical intervention (laser phototherapy, cryotherapy, vitrectomy)
21
Q
BLEPHARITIS
what are the causes?
A
meibomian gland dysfunction (common, posterior blepharitis)
seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).
22
Q
CATARACTS
what are the risk factors?
A
Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia
23
Q
CATARACTS
what is the clinical presentation?
A
usually asymmetrical, as both eyes are affected separately.
SYMPTOMS
It presents with:
- gradual painless loss of vision
- difficulty reading/watching TV
- Progressive blurring of the vision
- Colours becoming more faded, brown or yellow
- Starbursts (haloes around lights) can appear around lights, particularly at night
SIGNS
- loss of red reflex
- brown/white appearance of lens on slit-lamp
24
Q
CATARACTS
what are the investigations and findings?
A
Loss of the red reflex is a key examination finding.
The lens can appear grey or white using an ophthalmoscope, even from a distance. This is also seen on photographs taken with a flash.
25
CATARACTS
what are the complications of cataract surgery?
endophthalmitis
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
26
CENTRAL RETINAL ARTERY OCCLUSION
what are the causes?
main cause is atherosclerosis (causes an embolism)
others = giant cell arteritis,
27
CENTRAL RETINAL ARTERY OCCLUSION
what are the risk factors?
- smoking
- HTN
- diabetes
- raised cholesterol
- white
- older age
- male
- polymyalgia rheumatica
28
CENTRAL RETINAL ARTERY OCCLUSION
what is the clinical presentation?
typically sudden, painless, monocular vision loss occurring over seconds
patients may report transient vision loss prior to event (amaurosis fugax)
SYMPTOMS
- sudden painless vision loss in one eye
SIGNS
- reduced visual acuity
- afferent pupillary defect
- pale retina and 'cherry red spot' on fundoscopy
29
CENTRAL RETINAL ARTERY OCCLUSION
what is the management?
1st line
- reperfusion therapy (PENTOXIFYLLINE or HYPERBARIC OXYGEN)
- reduction in intraocular pressure (ACETAZOLAMIDE)
- IV methylprednisolone
- thrombolytic therapy (tissue plasminogen activator)
2nd line
- surgical intervention
long term management
- reduction in CVD risk (weight loss, aspirin + statins)
- inform DVLA
30
CONJUNCTIVITIS
what is the clinical presentation?
SYMPTOMS
- itchiness in one or both eyes
- conjunctival injection (redness)
- discharge (bacterial = purulent, viral = watery)
- difficulty opening eyes in morning (due to crusting)
SIGNS
- conjunctival follicles
- superficial punctate keratopathy
- periauricular lymph nodes
NO PAIN, PHOTOPHOBIA OR REDUCED VISUAL ACUITY
31
what are the differentials for a painful red eye?
Acute angle-closure glaucoma
Anterior uveitis
Scleritis
Corneal abrasions or ulceration
Keratitis
Foreign body
Traumatic or chemical injury
32
what are the differentials for painless red eye?
Conjunctivitis
Episcleritis
Subconjunctival haemorrhage
33
CONJUNCTIVITIS
what is the management?
1st line
- watch and wait (most resolve in 7 days)
- practice good hygiene
- no exclusion period required
- artificial tears
- mast cell stabilisers (in allergic conjunctivitis)
2nd line = topical antibiotics
- chloramphenicol 0.5% eye drops (2hrly for 2 days, then QDS for 5 days)
- chloramphenicol 1% ointment (QDS for 2 days, then BD for 5 days)
- fusidic acid 1% eye drops (2nd line, BD for 7 days)
34
DIABETIC RETINOPATHY
what is the pathophysiology?
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
35
DIABETIC RETINOPATHY
what are the key features of non-proliferative diabetic retinopathy?
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots ('soft exudates' - represent areas of retinal infarction),
venous beading/looping
intraretinal microvascular abnormalities (IRMA)
36
DIABETIC RETINOPATHY
what are the key 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
37
DIABETIC RETINOPATHY
what are the key features of maculopathy diabetic retinopathy?
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
38
DIABETIC RETINOPATHY
what are the complications?
Vision loss
Retinal detachment
Vitreous haemorrhage (bleeding into the vitreous humour)
Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma
Optic neuropathy
Cataracts
39
DIABETIC RETINOPATHY
what is the management for non-proliferative diabetic retinopathy?
regular observation
if severe/very severe consider panretinal laser photocoagulation
40
DIABETIC RETINOPATHY
what is the management for maculopathy diabetic retinopathy?
if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors
41
DIABETIC RETINOPATHY
what is the management for proliferative diabetic retinopathy?
Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels
Anti-VEGF medications by intravitreal injection
Surgery (e.g., vitrectomy) may be required in severe disease
42
KERATITIS
what are the causes?
Viral infection (e.g., herpes simplex = most common)
Bacterial infection (e.g.,
Pseudomonas or Staphylococcus)
Fungal infection (e.g., Candida or Aspergillus)
Contact lens-induced acute red eye (CLARE)
Exposure keratitis, caused by inadequate eyelid coverage (e.g., ectropion)
43
KERATITIS
what are the clinical features?
red eye: pain and erythema
photophobia
foreign body sensation , gritty sensation
hypopyon may be seen
44
KERATITIS
what are the investigations?
an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis
45
KERATITIS
what is the management?
stop using contact lens until the symptoms have fully resolved
topical antibiotics (quinolones = first-line)
cycloplegic for pain relief
e.g. cyclopentolate
46
KERATITIS
what are the complications?
corneal scarring
perforation
endophthalmitis
visual loss
47
HERPES KERATITIS
what is the pathophysiology?
Herpes simplex keratitis usually affects only the epithelial layer of the cornea
48
HERPES KERATITIS
what is the clinical presentation of primary and recurrent herpes keratosis?
Primary infection often involves mild symptoms of blepharoconjunctivitis (inflammation of the eyelid margins and conjunctiva).
Recurrent infection may present with:
Painful red eye
Photophobia
Vesicles (fluid-filled blisters)
Foreign body sensation
Watery discharge
Reduced visual acuity
49
HERPES KERATITIS
what are the investigations?
Slit lamp examination is required to diagnose keratitis.
Fluorescein staining shows a dendritic corneal ulcer. Dendritic describes the branching appearance of the ulcer.
Corneal scrapings can be used for viral testing.
50
HERPES KERATITIS
what is the management?
Patients should be referred for urgent assessment and management by an ophthalmologist.
Specialist management involves topical or oral antivirals (e.g., aciclovir or ganciclovir).
Corneal transplant is an option to treat permanent scarring and vision loss after keratitis.
51
OPTIC NEURITIS
what are the causes?
- multiple sclerosis: the commonest associated disease
- diabetes
- syphilis
52
OPTIC NEURITIS
what are the clinical features
- acute painful vision loss
- periocular pain, particularly on eye movement
- unilateral decrease in visual acuity over hours or days
- poor discrimination of colours, 'red desaturation' (dyschromatopsia)
- relative afferent pupillary defect
- central scotoma
53
OPTIC NEURITIS
what are the investigations?
- visual function tests = acuity, colour vision + visual fields
- MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
- lumbar puncture = if MS is considered
54
OPTIC NEURITIS
what is the management?
high-dose steroids = IV methylprednisolone
recovery usually takes 4-6 weeks
55
RETINAL DETACHMENT
what are the risk factors?
Lattice degeneration (thinning of the retina)
Posterior vitreous detachment
Trauma
Diabetic retinopathy
Retinal malignancy
Family history
56
RETINAL DETACHMENT
what is the clinical presentation?
SYMPTOMS
- floaters (dots, lines or haze)
- recurrent flashes
- painless
- progressive vision loss (starts at periphery + progresses towards centre)
- blurred vision
SIGNS
- decreased visual acuity
- peripheral visual field loss
- relative afferent pupillary defect
- fundoscopic findings (asymmetric red reflex, detached retinal folds appear pale, opaque + wrinkled)
57
RETINAL DETACHMENT
what are the investigations?
- slit lamp
- fundoscopy
to consider
- B-scan ultrasonography
- CT/MRI orbit
58
RETINAL DETACHMENT
what is the management?
immediate referral to ophthalmologist, should be seen within 24hrs
SURGERY
- vitrectomy
- scleral buckle
- pneumatic retinopexy
59
SCLERITIS
what are the causes?
- idiopathic = most common
- systemic conditions - RA, vasculitis (granulomatosis with polyangiitis)
- infection - pseudomonas or s.aureus
- ocular trauma
- ocular surgery
- systemic infection
60
SCLERITIS
what is the clinical presentation?
SYMPTOMS
- severe eye pain (worse on eye movement, can awaken from sleep)
- red eye
- eye watering (but no other discharge)
- photophobia
- blurred vision
- may have history of recurrent episodes
SIGNS
- red eye (do not blanch with phenylephrine + not mobile)
- visual acuity normal or reduced (depends on severity)
61
SCLERITIS
what are the risk factors?
rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis
62
SCLERITIS
what is the management?
1st line
- NSAIDS (ibuprofen 400mg TDS)
- corticosteroids (topical, oral or IV)
REFRACTORY CASES
- DMARDs (methotrexate, ciclosporin)
- biological agents (infliximab)
- surgical intervention
63
THYROID EYE DISEASE
what is the pathophysiology?
it is thought to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation
the inflammation results in glycosaminoglycan and collagen deposition in the muscles
64
THYROID EYE DISEASE
how can it be prevented?
smoking is the most important modifiable risk factor for the development of thyroid eye disease
radioiodine treatment may increase the inflammatory symptoms seen in thyroid eye disease. Prednisolone may help reduce the risk
65
THYROID EYE DISEASE
what is the clinical presentation?
the patient may be eu-, hypo- or hyperthyroid at the time of presentation
exophthalmos
conjunctival oedema
optic disc swelling
ophthalmoplegia
inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
66
THYROID EYE DISEASE
what is the management?
smoking cessation
topical lubricants may be needed to help prevent corneal inflammation caused by exposure
steroids
radiotherapy
surgery
67
THYROID EYE DISEASE
what are the complications?
exposure keratopathy
optic neuropathy
strabismus
diplopia
68
ORBITAL CELLULITIS
what is the most common cause?
It is usually caused by a spreading upper respiratory tract infection from the sinuses and carries a high mortality rate.
Most common bacterial causes - Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
69
ORBITAL CELLULITIS
what is the clinical presentation?
SYMPTOMS
- swelling and redness of eyelids
- pain on ocular movement
- diplopia
- fever
- malaise
SIGNS
- restricted ocular motility (ophthalmoplegia)
- RAPD
- chemosis
- proptosis
- reduced visual acuity
- impaired colour vision
- ptosis
70
ORBITAL CELLULITIS
what are the investigations?
- FBC = leukocytosis
- CRP = elevated
- blood cultures
- VBG = acidosis + raised lactate
- CT orbit + sinuses with contrast
to consider
- swab
- MRI
71
ORBITAL CELLULITIS
what is the management?
MEDICAL MANAGEMENT
- hospital admission
- elevation of head of the bed
- regular neurological + eye observations
- analgesia
- IV antibiotics (IV CO-AMOXICLAV or CEFTRIAXONE (clindamycin + metronidazole if penicillin allergic))
- topical decongestants
- daily ophthalmology + ENT reviews
SURGICAL MANAGEMENT
- surgical drainage +/- sinus washout
- lateral canthotomy
72
PREORBITAL CELLULITIS
what are the investigations?
Bloods - raised inflammatory markers
Swab of any discharge present
Contrast CT of the orbit may help to differentiate between preseptal and orbital cellulitis. It should be performed in all patients suspected to have orbital cellulitis
73
PREORBITAL CELLULITIS
what is the management?
All cases should be referred to secondary care for assessment
Oral antibiotics are frequently sufficient - usually co-amoxiclav
Children may require admission for observation
74
STYE
what is it?
Hordeolum externum is an infection of the glands of Zeis or glands of Moll.
The glands of Moll are sweat glands at the base of the eyelashes.
The glands of Zeis are sebaceous glands at the base of the eyelashes.
A stye causes a tender red lump along the eyelid that may contain pus
75
STYE
how is it managed?
treated with hot compresses and analgesia.
Topical antibiotics (e.g., chloramphenicol) may be considered if it is associated with conjunctivitis or if symptoms are persistent.
76
CHALAZION
what is it?
A chalazion occurs when a Meibomian gland becomes blocked and swells. It is often called a Meibomian cyst.
77
ENTROPION
what is the management?
INITIAL MANAGEMENT
- taping (must use lubricating eye drops)
DEFINITIVE MANAGEMENT
- surgical repair
78
ECTROPION
what is the management?
Mild cases may not require treatment.
Regular lubricating eye drops are used to protect the surface of the eye.
More significant cases may require surgery to correct the defect.
A same-day referral to ophthalmology is required if there is a risk to sight
79
TRICHIASIS
what is it?
Trichiasis refers to inward growth of the eyelashes. It results in pain and can cause corneal damage and ulceration.
80
CORNEAL ABRASIONS
what is the clinical presentation?
Painful red eye
Photophobia
Foreign body sensation
Epiphora (excessive tear production)/lacrimation
Blurred vision
81
CORNEAL ABRASIONS
what are the investigations?
fluorescein staining
- examination typically reveals a yellow-stained abrasion (representative of the de-epithelialized surface) which is usually visible to the naked eye
- visualisation is enhanced by the use of a cobalt blue filter (available on an ophthalmoscope) or a Wood's lamp
82
CORNEAL ABRASIONS
what is the management?
a topical antibiotic is recommended for these patients in order to prevent secondary bacterial infection.
83
OCULAR TRAUMA
what is hyphema?
blood in the anterior chamber of the eye
84
OCULAR TRAUMA
what is the risk of hyphema?
raised intraocular pressure which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes.
85
OCULAR TRAUMA
what is the management of hyphema?
Strict bed rest is required as excessive movement can redisperse blood that had previously settled; therefore high-risk cases are often admitted.
Even isolated hyphema will require daily ophthalmic review and pressure checks initially as an outpatient.
86
OCULAR TRAUMA
what is the management of orbital compartment syndrome?
urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit
87
SUBCONJUNCTIVAL HAEMORRHAGE
what are the causes?
cause is most commonly traumatic followed by spontaneous idiopathic cases, Valsalva manoeuvres and several systemic diseases.
88
SUBCONJUNCTIVAL HAEMORRHAGE
what are the risk factors?
Trauma and contact lens usage (68%): these are the most common causes generally, as well as being often the sole risk factor in younger patients
Idiopathic
Valsalva manoeuvre e.g. coughing, straining
Hypertension
Bleeding disorders
Drugs such as aspirin, NSAIDs and anticoagulants
Diabetes
Arterial disease and hyperlipidaemia
89
POSTERIOR VITREOUS DETACHMENT
what is it?
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
90
POSTERIOR VITREOUS DETACHMENT
what are the risk factors?
- increasing age
- highly myopic
91
POSTERIOR VITREOUS DETACHMENT
what are the symptoms?
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)
92
POSTERIOR VITREOUS DETACHMENT
what are the signs?
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
93
POSTERIOR VITREOUS DETACHMENT
what are the investigations?
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.
94
VITREOUS HAEMORRHAGE
what are the common causes?
proliferative diabetic retinopathy (over 50%)
posterior vitreous detachment
ocular trauma: the most common cause in children and young adults
95
VITREOUS HAEMORRHAGE
what are the symptoms?
painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision
96
VITREOUS HAEMORRHAGE
what are the investigations?
dilated fundoscopy: may show haemorrhage in the vitreous cavity
slit-lamp examination: red blood cells in the anterior vitreous
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury
97
CORNEAL FOREIGN BODY
what are the indications for referral to ophthalmology?
Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns)
Significant orbital or peri-ocular trauma has occurred.
A chemical injury has occurred (irrigate for 20-30 mins before referring)
Foreign bodies composed of organic material (such as seeds, soil) should be referred to ophthalmology as these are associated with a higher risk of infection and complications
Foreign bodies in or near the centre of the cornea
Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity.
98
OPTIC ATROPHY
what are the 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
99
OPTIC ATROPHY
what are the 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)
100
SUDDEN LOSS OF VISION
what are the causes?
- ischaemic (amaurosis fugax)
- central retinal vein occlusion
- central retinal artery occlusion
- vitreous haemorrhage
- retinal detachment
101
RETINAL VEIN OCCLUSION
what are the risk factors?
Hypertension
High cholesterol
Diabetes
Smoking
High plasma viscosity (e.g., myeloma)
Myeloproliferative disorders
Inflammatory conditions (e.g., SLE)
102
RETINAL VEIN OCCLUSION
what is the clinical presentation?
SYMPTOMS
- blurred vision
- painless
- unilateral and sudden
- metamorphopsia (image distortion)
SIGNS
- stormy sunset appearance on fundoscopy (vascular dilatation + tortuosity, dot + flame haemorrhages, cotton wool spots, macular oedema)
- relative afferent pupillary defect
103
RETINAL VEIN OCCLUSION
what is the pathophysiology?
Blockage of a retinal vein causes venous congestion in the retina. Increased pressure in the retinal veins results in fluid and blood leaking into the retina, causing macular oedema and retinal haemorrhages. This results in retinal damage and vision loss.
104
RETINAL VEIN OCCLUSION
what are the fundoscopic findings?
Dilated tortuous retinal veins
Flame and blot haemorrhages
Retinal oedema
Cotton wool spots
Hard exudates
105
RETINAL VEIN OCCLUSION
what is the management?
UNCOMPLICATED CRVO
- observe + manage risk factors
EVIDENCE OF MACULAR OEDEMA
- intravitreal VEGF inhibitor
- intravitreal corticosteroid injections
EVIDENCE OF NEOVASCULARISATION
- panretinal photocoagulation
106
VISUAL FIELD DEFECTS
where is the location if there is bitemporal hemianopia where upper quadrant defect > lower quadrant defect?
inferior chiasm - pituitary tumour
107
VISUAL FIELD DEFECTS
where is the location if there is bitemporal hemianopia where lower quadrant defect > upper quadrant defect?
superior chiasm - craniopharyngioma
108
VISUAL FIELD DEFECTS
where is the lesion located in a inferior homonymous quadrantanopia?
Baum's loop in parietal lobe
109
VISUAL FIELD DEFECTS
where is the lesion located in a superior homonymous quadrantanopia?
Meyers loop in the temporal lobe
110
VISUAL FIELD DEFECTS
where is the lesion in left homonymous hemianopia with macular sparing?
calcarine sulcus
111
UVEITIS
what are the clinical features of intermediate uveitis?
SYMTPOMS
- worsening floaters
- decreased vision
SIGNS
- vitreous haze
- snowballs
- macular oedema
112
UVEITIS
what are the clinical features of posterior uveitis?
SYMPTOMS
- decreased vision
- visual field changes
SIGNS
- chorioretinal lesions
- retinal whitening
113
UVEITIS
what are the investigations?
PHYSICAL EXAMINATION
- visual fields
- visual acuity
- cranial nerve assessment
- reflexes
SLIT LAMP
- snowballs = intermediate
- retinal whitening = posterior
to consider
- infection/autoimmune screen
114
UVEITIS
what is the management?
- assessment with ophthalmologist within 24hrs
1st line
- corticosteroids (topical, oral, IV or ocular injections)
- antimicrobials (if fungal/bacterial/viral source suspected)
2nd line
- immunosuppressant +/- DMARDs
- surgical intervention (laser phototherapy, cryotherapy or vitrectomy)
115
UVEITIS
what are the complications?
- visual loss or impairment
- secondary cataracts or glaucoma
- retinal detachment
- vitreous haemorrhage
116
ACUTE ANGLE CLOSURE GLAUCOMA
what are the investigations?
must be urgently referred to ophthalmologist
- slit lamp = shallow anterior chamber, optic disc cupping, optic disc pallor
- gonioscopy (GOLD STANDARD)
- tonometry
117
OPEN-ANGLE GLAUCOMA
what are the fundoscopic findings?
- optic disc cupping
- bayonetting of vessels
- cup notching
- optic disc pallor
- disc haemorrhages
118
GLAUCOMA MEDICATIONS
what are the side effects of miotics (e.g. pilocarpine)?
- constricted pupil
- retinal detachment
- vitreous haemorrhage
- headache
119
GLAUCOMA MEDICATIONS
what are the side effects of carbonic anhydrase inhibitors (e.g. acetazolamide)?
- dry mouth
- change in taste
- tingling feeling in extremities
- stevens-johnson syndrome
not for long term use orally
do not use in hyperchloremic acidosis or sulphonamide sensitivity
120
GLAUCOMA MEDICATIONS
how does prostaglandin analogues (e.g. latanoprost) work?
increases the uveosceral outflow of aqueous humour
121
GLAUCOMA MEDICATIONS
how do prostamides (e.g. bimatoprost) work?
increases uveoscleral outflow of aqueous humour and acts via trabecular meshwork
122
GLAUCOMA MEDICATIONS
how do beta-blockers (e.g. timolol) work?
decreases aqueous humour production
123
GLAUCOMA MEDICATIONS
what are the side effects of beta-blockers (e.g. timolol)?
may cause corneal disorders
avoid in asthma + heart block
124
GLAUCOMA MEDICATIONS
how do sympathomimetics (e.g. brimonidine) work?
decreases aqueous humour production
125
GLAUCOMA MEDICATIONS
what are the side effects of sympathomimetics (e.g. brimonidine)?
- hyperaemia
- burning + stinging eyes
- dry mouth
avoid in CVD, raynauds + if taking MAOIs or TCAs
126
CENTRAL RETINAL ARTERY OCCLUSION
what are the investigations?
- ESR/CRP (to investigate temporal arteritis)
to consider
- vasculitis screening
- coagulation screen
- HbA1c/lipid profile
127
CONJUNCTIVITIS
what are the causes?
BACTERIA
- s.aureus
- h.influenzae
- s.pneumoniae
- chlamydia + n.gonorrhoeae
VIRUSES
- adenovirus
- coxsackie
- enterovirus
- herpes simplex (HSV)
NON-INFECTIVE
- allergic conjunctivitis
128
ORBITAL CELLULITIS
what are the complications?
- central retinal artery or vein occlusion
- optic neuropathy
- endophthalmitis
- subperiosteal abscess
- meningitis
- cavernous sinus thrombosis
- cerebral abscess
129
SCLERITIS
what are the investigations?
- baseline bloods (FBC, U&Es, LFTs, bone profile)
- ESR + CRP
- autoimmune screen
- urine dipstick
- B scan ultrasonography
130
ANTERIOR UVEITIS
what is the pathophysiology?
pain is due to irritation of ciliary nerves
photophobia is due to irritation of trigeminal nerve from ciliary spasm
131
STYE
what are the clinical features?
painful red hot lump on eyelid that points outwards
causes localised inflammation
132
FUNDOSCOPY
what does this show?
pre-proliferative diabetic retinopathy
133
FUNDOSCOPY
what does this show?
age related macular degeneration
134
FUNDOSCOPY
what does this show?
branch retinal vein occlusion
135
FUNDOSCOPY
what does this show?
central retinal artery occlusion
136
FUNDOSCOPY
what does this show?
central retinal artery occlusion
137
FUNDOSCOPY
what does this show?
central retinal vein occlusion
138
FUNDOSCOPY
what does this show?
retinal branch vein occlusion
139
FUNDOSCOPY
what does this show?
proliferative diabetic retinopathy
140
FUNDOSCOPY
what does this show?
pre-proliferative diabetic retinopathy
141
FUNDOSCOPY
what does this show?
panretinal photocoagulation
142
FUNDOSCOPY
what does this show?
papilloedema
