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Year 4 - Neuro and Special Senses > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

What are some of the characteristics of diabetic retinopathy

A

A- (micro) Aneurysms

B - Blot Haemorrhages

C- Cotton wool spots

D - Deposits

E - (hard) Exudates

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2
Q

What are the different classifications of diabetic retinopathy?

How are they managed?

A

Non proliferate

Pre proliferative

Proliferative - pan retinal photocoagulation within 2 weeks

Maculopathy - focal and grid laser

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3
Q

What are the differnet types of diabetic maculopathy? How are the managed

A
  • Focal. Mx: focal laser
  • Diffuse. Mx: grid laser
  • Ischaemic. Mx: observe
  • CSMO (clinically significant macular oedema):
  • Mixed - diffuse + ischaemic Central involving
  • Central involving: anti VEGF therapies. IV illuvien
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4
Q

What are the complications of diabetic retinopathy

A
  • Retinal detachment
  • Cataracts
  • Vitreous haemorrhage
  • Optic neuropathy
  • Rebeosis iridis: new blood vessel formation in the iris
  • Others: neovascular glaucoma, third nerve palsies, idiotpathy, orbital infection
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5
Q

How is diabetic retinopathy managed?

A
  • Conservative: BP control, good glycemic control, diet, exercise, reduce cholesterol (statin), stop smoking, moderate alcohol intake
  • Medical:
    • Background: annual screening
    • Pre proliferative: W+W
    • Proliferative (active): pan-retinal photo coagulation in 2 weeks
    • Proliferative stable: FU 4-6 months
    • Proliferative with DMO: macular laser and PRP
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6
Q

How is rubeosis iriditis mx (2nd to diabetic retinopathy)

A
  • Urgent pan retinal photo coagulation
  • Vit haemorrhage: vitrectomy + endolaser
  • Rubeotic glaucoma: IOP reduction, victrectomy, anti VEGF, pan retinal photocogulation
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7
Q

What are the causes of painful vs pain less red eye

A
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8
Q

What is glaucoma?

A

A group of conditions characterised by increased raised intraocular pressure giving rise to changes around the head of the optic disc and corresponding visual field defects

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9
Q

What type of vision does glaucoma affects?

What type of visual defect is seen?

A

Peripheral

Arcuate scotoma

First in the nasal field

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10
Q

What are the RFs for open angle glaucoma

A
  • Black ethnicity
  • Age
  • Diabetes
  • FH/ genetics
  • Hypertension
  • Corticosteroids
  • Myopia
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11
Q

Describe the pathophysiology of open angle glaucoma?

A
  • Aqueous humour: produced by the ciliary body, flows through the anterior chamber, through the trabecular meshwork into the canal of schlemm
  • Open angle: gradual increased resistance from the trabecular meshwork which makes it difficult for the aq. humour to drain through
  • This results in increased IOP in the anterior chamber
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12
Q

How does open angle glaucoma present?

A
  • Chronic, progressive reduced peripheral vision: nasal scotoma progressing to tunnel vision
  • Nasal and superior fields are lost first
  • Worse at night: haloes, pain, headache, blurred vision
  • Reduced visual acuity
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13
Q

How is open glaucoma monitored?

What are the IOPs?

A
  • Slit lamp: fundoscopy
  • Tonometry: 10-21 (mean of 16)
    • Non contact
    • Goldmann Applanation Tonometry
  • Visual field assessment
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14
Q

What characteristics are seen on fundoscopy of open angle glaucoma

A
  • Optic disc: cupping, pallor, notching
  • Bayonetting of vessels (vessel breaks)
  • Disc haemorrhages
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15
Q

How is open angle glaucoma managed?

A

Medical Mx

  • Prostaglandin analogues: latanoprost
  • Beta blockers: timolol
  • Sympathomimetics: brimonidine
  • Carbonic anhydrase inhibitors: dorzalamide

Surgery

  • Argon laser trabeculoplasty
  • Selective laser trabeculoplasty
  • Definitive: peripheral laser iridotomy
  • Surgery: trabeculectomy : filtering bleb
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16
Q

What are the RFs of acute angle glaucoma?

A
  • age
  • female
  • chinese
  • shallow anterior chamber
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17
Q

What medications can cause acute open angle glaucoma

A
  • Anti cholinergics
  • Antiadrenergics
  • Trycyclics
  • Mydiatric eye drops
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18
Q

How does closed angle glaucoma present?

A
  • Painful red eye
  • N+V, headache
  • Haloes around light
  • Sx worse at night/ worse with mydriasis (watching TV in a dark room)
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19
Q

When examining acute open angle glaucoma how does it appear?

A
  • Red eye, tear
  • Hazy cornea
  • Reduced visual acuity
  • Ciliary injection
  • Cornea: oedema and firm on palpation
  • Semi dilated un reactive pupil
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20
Q

How is acute angle closure glaucoma managed?

A
  • Lie pt on back
  • 500mg IV acetozolamide injection
  • Topical therapy: Pilocarpine drops 2%, timolol 0.5%
  • anti emetic and analgesic
  • Definitive: peripheral laser iridotomy
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21
Q

What are some of the complications of angle closure glaucoma:

A

Central retinal artery/ vein occlusion

Blindness

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22
Q

What conditions are associated with anterior uveitis?

A

HLA B27 +ve: reactive arthritis, ank. spond, IBD

Sarcoidosis

Syphilus

TB

HSV

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23
Q

How does anterior uveitis present?

A

Appearance

  • Mid constricted pupil (miosis)
  • Ciliary flush
  • Acute, painful red eye: conjunctival injection
  • Hypopyon
  • Flashers and floaters

Sx: photophobia, pain on eye movement, Lacrimation

Reduced visual acuity

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24
Q

How is anterior uveitis investigated and managed?

A
  • Ix: slit lamp, fundoscopy
  • Mx: steroid eye drops (pred/ dex)
    • cycloplegic eye drops (cyclopentate + atropine) - ANTI MUSCARINICS
    • Severe: victrectomy, laser/ cryotherapy
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25
Q

What is episcleritis and who does it usually affect? What are its associated?

A
  • self limiting inflammation of the episclera (outermost layer of the sclera)
  • Who: young + middle aged adult, not always by infection
  • Associations: IBD + RA
  • 50% bilaterla
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26
Q

How does epicleritis present?

A
  • Painless, red eye - Patch of segmental redness
  • No loss of visual acuity, no discharge
  • Foreign body sensation
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27
Q

How is episcleritis managed?

A
  • Lubricating eye drops, simple analgesia, cold compresses
  • Severe: NSAIDs, topical steroid drops
28
Q

How does scleritis present?

A
  • Painful red eye
  • Photophobia
  • Pain with ocular movemetns
  • Reduce visual acuity
  • Abnormal pupil reaction to light
29
Q

How is scleritis managed?

A
  • Urgent referral
  • NSAIDs, steroids, immunosuppression
30
Q

How do corneal abrasions present?

How are they managed?

A

foreign body sensation

watering eye

photophobia

Mx: analgesia, lubricating eye drops

abx eye drops: chloramphenicol

Cyclopentate eye drops: good for photophobia

FU in 1/52

31
Q

How does keratitis present?

A
  • Red eye: pain, erythema
  • Photophobia
  • Foreign body sensation
  • Hypopyon
  • Reduced visual acuity
32
Q

How is keratitis investigated and managed?

What are some of its complications

A
  • Ix: slit lamp + floreescein staining, corneal swabs + scraping
  • Mx: contact lens users - stop use till sx resolve
  • Topical abx: levofloxacin
  • Steroid eye drops + cyclopentate eye drops (for photophobia)
  • Complications: perforation, scarring, enopthalmitis, visual loss
33
Q

How does herpes simplex keratitits present and how is it managed?

A
  • Red painful eye, photophobia, epiphora, reduced visual acuity
  • Mx: topical aciclovir 10-14 days, cyclopentate + topical steroid drops
34
Q

What are the causes of

A
35
Q

What is Herpes Zoster Ophthalmicus?

How is it mxd?

A
  • Eye involvement more likely if lesions on tip if nose or at medial canthus
  • Conjunctivitis, keratitis, uveitis, trabeculitis, retinitis, optic neuritis
  • MX: Give oral antiviral (acyclovir 800mg 5 x per day for 7 days)
    • Refer to Rapid Access Clinic if eye red or vision blurred
36
Q

How is viral conjunctivitis mxd?

A
  • Mx: Antihistamines (oral or topical): azelastinem olopatadine
  • Topical mast-cell stabiliser
37
Q

What is chlamydial conjunctivitis?

How is it ixd + mxd?

A
  • Consider in sexually active adolescents/ adults (+/- genital infection) + chronic with a mild keratitis
  • Symptoms/Signs: Usually unilateral, FB sensation, Lid crusting with sticky discharge, follicles
    • No response with topical antibiotics
  • Ix: Swab/ smear; Direct monoclonal fluorescent antibody microscopy; PCR
  • Mx: Treatment- topical tetracycline/ oral doxycycline/ azithromycin
    • Contact trace + GUM referral
38
Q

What are some of the causes of sudden loss of vision?

A
  • Ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc): CR (central retinal) A/V occlusion
  • Vitreous haemorrhage
  • Retinal detachment
  • Retinal migraine
  • Wet AMD
39
Q

What are some of the causes of painful loss of vision?

A
  • Acute glaucoma
  • Severe corneal pathology
  • Severe uveitis
  • Endopthalmitis
  • Optic neuritis
40
Q

What is Ischaemic/vascular: aka ‘amaurosis fugax’?

How is it ixd / mxd?

A
  • Altitudinal field defects are often seen: ‘curtain coming down’
  • Ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve
  • Wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypoperfusion
  • Fundoscopy: plain, swollen optic disc
  • May represent a TIA hence mx: aspirin 300mg
41
Q

What are the sx of GCA?

A
  • Sx: new onset headache, malaise, jaw/ tongue claudication (chewing pain), +/- tender scalp (brushing hair; look for shingles rash 1st) and temporal arteries, neck pain
  • Vision loss: unilateral (rarely bilateral) – perm. Can be precipitated by amaurosis fugax
  • Transient blurring, diplopia, reduced acuity
42
Q

How is GCA ixd + mxd?

A
  • Ix: raised PV, ESR, CRP, FBC (raised platelets) and temporal artery biopsy
  • Mx: prednisolone 60mg + PPI (take bloods first)
43
Q

What is CRVO? Mx?

A
  • Sx: sudden onset, painless blurring of unilateral vision
  • Incidence increases with age, more common than arterial occlusion
  • Causes: glaucoma, polycythaemia, hypertension, age
  • Fundoscopy: Severe retinal haemorrhages (flame)
  • Mx: refer to on call ophthalmologist, retinal photocoagulation (if retinal ischaemia has caused neovascularisation
    • Anti VEGF: to treat macular oedema
    • 2nd: macular laser
44
Q

What is Central Retinal Artery Occlusion?

A
  • Sx: Sudden painless loss of vision (in seconds)
    • Reduced visual acuity - finger counting or worse,
    • RAPD
  • Fundoscopy: ‘cherry red’ macula spot on a pale retina
  • Mx:
    • Restore blood flow – ocular massage, surgery: removal of aqueous from anterior chamber
    • Inhaling carbogen (a mixture of 5% carbon dioxide and 95% oxygen) to dilate the artery
    • Sublingual isosorbide dinitrate to dilate the artery
45
Q

What are some of the causes of optic neuritis?

What are the features?

How is it ixd + mxd?

A

Demyelination (MS + MG), diabetes, syphilis, viral (herpes), infections (CSD)

Features

  • unilateral decrease in visual acuity over hours or days
  • reduced color vision, ‘red desaturation’
  • pain worse on eye movement
  • RAPD
  • Central scotoma (blind spot larger)

Ix: MRI for demyelination

Mx: high-dose steroids (methylprednisolone then pred), recovery usually takes 4-6 weeks

46
Q

What are some of the cause of flashers and floaters?

A

Flashes

  • Migraine – fortified spectra fo spreading zig zag lines, not accompanies by floaters, ask about N+V, headache, PMH/ FH migraines
  • Retinal pathology – peripheral and harder to see. Can be caused by vitreous detachment.

Floaters

  • Blood: vitreous haemorrhage (causes: diabetic retinopathy, trauma, vein occlusions, retinal tear/ traction on a retinal vessel
  • Inflammation: intermediate, posterior or panevetitis
  • Infection: bacterial of fungal endopthalmitis
  • Intraocular malignancy
    • Mx: examine vitreous and retina. 24h assessment
47
Q

What are some causes of vitreous haemorrhage?

A

diabetes, bleeding disorders, anticoagulants, ocular trauma (kids); posterior vitreous detachment

48
Q

What are some of the features + signs of vitreous haemorrhage? Ix, Mx?

A

Features

  • Sudden painless visual loss/ haze,
  • Floaters or shadows/ dark spot
  • Red hue in vision

Signs:

  • Decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
  • Visual field defect if severe haemorrhage
  • Large haemorrhages can completely occlude vision and lead to loss of red reflex

Ix: dilated fundoscopy, slit lamp examination (RBCs in anterior vitreous), USS, fluorescein angiography, orbital CT (to identify globe injury)

Mx: surgery: vitrectomy

49
Q

How does retinal detachment present?

A
  • Presentation: 4 Fs: flashers, floaters, field loss and fall in acuity – curtain falling over vision. Field defects indicate position and extent of detachment
    • Peripheral vision loss - sudden and like a shadow coming across the vision.
    • Blurred and distorted vision
  • Examination: Opthalmoscope: grey opalescent retina, ballooning forward, extensive retinal detachment will pull off the macula (this would cause central vision loss)
50
Q

How is retinal detachment mxd?

A

Mx: EMERGENCY.

  • Retinal tears: laser therapy/ cryotherapy
  • Surgery: victrectomy and gas/ oil tamponade (replacing it with oil or gas) + scleral silicone implants
  • Scleral buckling: uses a silicone buckle to apply pressure on the outside of the eye to bring choroid in and in contact with detached retina
  • Cryotherapy/ laser coagulation to secure retina
  • Pneumatic retinopexy: injects a gas bubble into vitreous body
51
Q

What is Posterior vitreous detachment?

A
  • Separation of the vitreous membrane from the retina. This occurs due to natural changes to the vitreous fluid of the eye with ageing.
  • Posterior vitreous detachment is a common condition that does not cause any pain or loss of vision. However, rarely the separation of the vitreous membrane can lead to tears and detachment of the retina.
52
Q

How does posterior vitreous detachment present?

A
  • The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
  • Flashes of light in vision
  • Blurred vision
  • Cobweb across vision
  • Appearance of a dark curtain descending down vision (means that there is also retinal detachment)

Signs: Weiss ring on ophthalmoscopy

53
Q

How is posterior vitreous detachment managed?

A
  • Investigations: 24h ophthalmologist referral to rule out retinal tears or detachment
  • Management:
    • Symptoms gradually improve over a period of around 6 months: no treatment is necessary.
    • Surgery to fix potential associated retinal tear or detachment
54
Q

What is the presentation of retinitis pigmentosa?

A
  • night blindness is often the initial sign
  • tunnel vision due to loss of the peripheral retina
  • fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
55
Q

What are some of the causes of transient loss of vision?

A
  • Amaurosis fugax/ TIA
  • Migraine
  • Papilledema
  • Cataract
  • Uveitis (NOT anterior – the others)
  • Glaucoma (open angle) – see above
  • Dry AMD
  • Diabetic retinopathy
56
Q

What are cataracts and what are some of its causes?

A
  • Common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy it more difficult for light to reach the back of the eye (retina), causing reduced/blurred vision.
  • Leading cause of curable blindness worldwide.
57
Q

What are some of the causes of cataracts?

A
  • Normal ageing process: most common cause
  • Other possible causes: Smoking, Increased alcohol consumption, Trauma, Diabetes mellitus, Long-term corticosteroids, Radiation exposure, Myotonic dystrophy, Metabolic disorders: hypocalcaemia, Downs syndrome
58
Q

What are some of the sx + signs of cataracts?

A
  • Reduced vision – clouded/ blurry
  • Faded colour vision: making it more difficult to distinguish different colours
  • Glare: lights appear brighter than usual
  • Halos around lights
  • Children: squint, nystagmus, amblyopia
  • Signs: Defect in the red reflex: Cataracts will prevent light from getting to the retina
59
Q

How are cataracts mxd?

A
  • Conservatively: prescribing stronger glasses/contact lens, or encouraging the use of brighter lighting.
  • Surgery: only effective mx: Involves removing the cloudy lens and replacing this with an artificial one. Lens extraction and intraocular lens implant
    • Lens extraction by phaeoemulsification (broken by USS and aspirated) and Perspex rolled out
    • Complicated or extracapsular extraction – larger incision needed
      • NICE: referral for surgery to be dependent upon whether a visual impairment is present, impact on quality of life, patient choice, bilateral and the possible risks and benefits of
      • Prior to cataract surgery, patients should be provided with information on the refractive implications of various types of intraocular lenses.
60
Q

What are some of the complications of cataract surgery?

A
  • Posterior capsule opacification: thickening of the lens capsule (peri op)
  • Retinal detachment
  • Posterior capsule rupture (late post op: Build up of debris on the capsule
    • Mx: YAG laser
  • Endophthalmitis: inflammation of aqueous and/or vitreous humour (early post op)
    • Presentation: Pain (usually), Worsening vision, Red injected eye, Occasionally hypopyon, Hazy cornea
61
Q

What is age related macular degeneration?

A
  • Degeneration in the macular (central retina) that cause a progressive deterioration in vision.
  • Most common cause of blindness in the UK
  • Key finding: drusen seen during fundoscopy.
  • Two types
    • Wet (dry) – 10%. Worse prognosis
    • Dry (90%). 90%
62
Q

What are some of the RFs of ARMD?

A

Age, Smoking, White or Chinese ethnic origin, Family history, CVSD (hypertension, dyslipidaemia, DM)

63
Q

What are drusen?

A
  • Caused by degeneration of retinal photoreceptors
  • They are yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane.
  • Some drusen can be normal: they are small (< 63 micrometres) and hard.
  • Early sign of macular degeneration: Larger and greater numbers of drusen. They are common to both wet and dry AMD (but mainly dry)
64
Q

What are the differences between dry and wet AMD?

What are some similarities?

A

Dry AMD – 90%

  • Also known as atrophic
  • Characterised by drusen - yellow round spots in Bruch’s membrane

Wet AMD – 10% - WORST PROGNOSIS

  • Also know as exudative or neovascular macular degeneration
  • Characterised by choroidal neovascularisation (into retina)
  • Leakage of serous fluid and blood from vessels -> oedema -> rapid loss of vision

Other fx in BOTH wet and dry AMD are:

  • Atrophy of the retinal pigment epithelium
  • Degeneration of the photoreceptors
65
Q

How does AMD present?

A
  • Gradual worsening central visual field loss
  • Reduced visual acuity
  • Crooked or wavy appearance to straight lines
  • Wet age-related macular degeneration presents more acutely.
  • Loss of vision over days and progress to full loss of vision over 2-3 years. Often progresses to bilateral disease.
  • Difficulty reading, making out faces, reduced night time vision
  • They may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects
66
Q

How is AMD ixd?

A
  • Snellen chart: Reduced acuity
    • Scotoma (a central patch of vision loss)
  • Amsler grid test – distortion of line perception
  • Fundoscopy: Drusen (late finding)
    • Wet AMD: fluid leakage, localised detachment of pigment and haemorrhage
  • Slit-lamp biomicroscopic fundus examination - identify any pigmentary, exudative or haemorrhagic changes affecting the retina
  • Optical coherence tomography: used to gain a cross-sectional view of the layers of the retina. Used to diagnose wet AMD.
  • Fluorescein angiography: ​oedema and neovascularisation (wet AMD) – can guide anti VEGF therapy
67
Q

How is AMD mxd?

A

Refer suspected cases to an ophthalmologist for assessment and management.

  • Dry AMD: no specific treatment.
    • Conservative (lifestyle): Avoid smoking, BP control, vitamin supplementation
  • Wet AMD
    • 1st line: Anti-VEGF medications: Medications e.g. ranibizumab, bevacizumab and pegaptanib – given via intravitreal injection
      • Vascular endothelial growth factor: involved in the development of new blood vessels in the retina.
      • Block VEGF and slow the development of new vessels.
      • Injected directly into the vitreous chamber of the eye once a month. Need to be started within 3 months to be beneficial.

Year 4 - Neuro and Special Senses (8 decks)

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