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OPHTHALMOLOGY Flashcards

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1
Q

OPEN-ANGLE GLAUCOMA
what are the risk factors?

A

increased age
family history
black
myopia (nearsighted)
hypertension + CVD
diabetes mellitus
corticosteroid use

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2
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)

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3
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
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4
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

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5
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.

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6
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)
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7
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
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8
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)

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9
Q

BLEPHARITIS
what are the causes?

A

meibomian gland dysfunction (common, posterior blepharitis)

seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).

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10
Q

CATARACTS
what are the risk factors?

A

Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia

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11
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

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12
Q

CATARACTS
what are the complications of cataract surgery?

A

endophthalmitis
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture

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13
Q

CENTRAL RETINAL ARTERY OCCLUSION
what is the management?

A

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

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14
Q

what are the differentials for a painful red eye?

A

Acute angle-closure glaucoma
Anterior uveitis
Scleritis
Corneal abrasions or ulceration
Keratitis
Foreign body
Traumatic or chemical injury

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15
Q

what are the differentials for painless red eye?

A

Conjunctivitis
Episcleritis
Subconjunctival haemorrhage

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16
Q

DIABETIC RETINOPATHY
what is the pathophysiology?

A

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

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17
Q

DIABETIC RETINOPATHY
what are the key features of non-proliferative diabetic retinopathy?

A

microaneurysms
blot haemorrhages
hard exudates
cotton wool spots (‘soft exudates’ - represent areas of retinal infarction),
venous beading/looping
intraretinal microvascular abnormalities (IRMA)

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18
Q

DIABETIC RETINOPATHY
what are the key features of proliferative diabetic retinopathy?

A

retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM

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19
Q

DIABETIC RETINOPATHY
what are the key features of maculopathy diabetic retinopathy?

A

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

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20
Q

DIABETIC RETINOPATHY
what are the complications?

A

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

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21
Q

DIABETIC RETINOPATHY
what is the management for non-proliferative diabetic retinopathy?

A

regular observation
if severe/very severe consider panretinal laser photocoagulation

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22
Q

DIABETIC RETINOPATHY
what is the management for maculopathy diabetic retinopathy?

A

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

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23
Q

DIABETIC RETINOPATHY
what is the management for proliferative diabetic retinopathy?

A

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

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24
Q

KERATITIS
what are the causes?

A

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)

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25
KERATITIS what are the clinical features?
red eye: pain and erythema photophobia foreign body sensation , gritty sensation hypopyon may be seen
26
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
27
KERATITIS what are the complications?
corneal scarring perforation endophthalmitis visual loss
28
OPTIC NEURITIS what are the causes?
- multiple sclerosis: the commonest associated disease - diabetes - syphilis
29
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
30
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
31
OPTIC NEURITIS what is the management?
high-dose steroids = IV methylprednisolone recovery usually takes 4-6 weeks
32
RETINAL DETACHMENT what are the risk factors?
Lattice degeneration (thinning of the retina) Posterior vitreous detachment Trauma Diabetic retinopathy Retinal malignancy Family history
33
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)
34
RETINAL DETACHMENT what is the management?
immediate referral to ophthalmologist, should be seen within 24hrs SURGERY - vitrectomy - scleral buckle - pneumatic retinopexy
35
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
36
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)
37
SCLERITIS what are the risk factors?
rheumatoid arthritis: the most commonly associated condition systemic lupus erythematosus sarcoidosis granulomatosis with polyangiitis
38
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
39
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
40
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
41
THYROID EYE DISEASE what are the complications?
exposure keratopathy optic neuropathy strabismus diplopia
42
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
43
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
44
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
45
CHALAZION what is it?
A chalazion occurs when a Meibomian gland becomes blocked and swells. It is often called a Meibomian cyst.
46
ENTROPION what is the management?
INITIAL MANAGEMENT - taping (must use lubricating eye drops) DEFINITIVE MANAGEMENT - surgical repair
47
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
48
CORNEAL ABRASIONS what is the management?
a topical antibiotic is recommended for these patients in order to prevent secondary bacterial infection.
49
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.
50
OCULAR TRAUMA what is the management of orbital compartment syndrome?
urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit
51
POSTERIOR VITREOUS DETACHMENT what are the risk factors?
- increasing age - highly myopic
52
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)
53
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).
54
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
55
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
56
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.
57
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
58
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)
59
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
60
UVEITIS what are the clinical features of intermediate uveitis?
SYMTPOMS - worsening floaters - decreased vision SIGNS - vitreous haze - snowballs - macular oedema
61
UVEITIS what are the clinical features of posterior uveitis?
SYMPTOMS - decreased vision - visual field changes SIGNS - chorioretinal lesions - retinal whitening
62
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
63
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)
64
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
65
OPEN-ANGLE GLAUCOMA what are the fundoscopic findings?
- optic disc cupping - bayonetting of vessels - cup notching - optic disc pallor - disc haemorrhages
66
GLAUCOMA MEDICATIONS what are the side effects of miotics (e.g. pilocarpine)?
- constricted pupil - retinal detachment - vitreous haemorrhage - headache
67
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
68
GLAUCOMA MEDICATIONS how does prostaglandin analogues (e.g. latanoprost) work?
increases the uveosceral outflow of aqueous humour
69
GLAUCOMA MEDICATIONS how do prostamides (e.g. bimatoprost) work?
increases uveoscleral outflow of aqueous humour and acts via trabecular meshwork
70
GLAUCOMA MEDICATIONS what are the side effects of beta-blockers (e.g. timolol)?
may cause corneal disorders avoid in asthma + heart block
71
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
72
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
73
SCLERITIS what are the investigations?
- baseline bloods (FBC, U&Es, LFTs, bone profile) - ESR + CRP - autoimmune screen - urine dipstick - B scan ultrasonography
74
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
75
FUNDOSCOPY what does this show?
pre-proliferative diabetic retinopathy
76
FUNDOSCOPY what does this show?
age related macular degeneration
77
FUNDOSCOPY what does this show?
branch retinal vein occlusion
78
FUNDOSCOPY what does this show?
central retinal artery occlusion
79
FUNDOSCOPY what does this show?
central retinal artery occlusion
80
FUNDOSCOPY what does this show?
central retinal vein occlusion
81
FUNDOSCOPY what does this show?
retinal branch vein occlusion
82
FUNDOSCOPY what does this show?
proliferative diabetic retinopathy
83
FUNDOSCOPY what does this show?
pre-proliferative diabetic retinopathy
84
FUNDOSCOPY what does this show?
panretinal photocoagulation
85
FUNDOSCOPY what does this show?
papilloedema

MY REVISION - ALL TO DO 2 (24 decks)

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