Ophthalmology Flashcards

1
Q

What happens in acute angle closure glaucoma?

A
  • Angle of anterior chamber narrows
  • Acute obstruction
  • Rapid intraocular pressure (IOP) >30mmHg (norm= 15-20)
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2
Q

What is the difference between Primary + Secondary acute angle closure glaucoma?

A

Primary: anatomical predisposition, e.g. narrow angle (Asians), thin iris, thick lens.
Secondary: traumatic haemorrhage, which pushes posterior chamber anteriorly.

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3
Q

What is the background anatomy associated with acute angle closure glaucoma?

A

Normal eye: ciliary body (behind iris) produces aqueous humor > drains into trabecular meshwork (angle between iris + cornea: anterior chamber angle)
AACG: Iris opposes trabecular meshwork > blocks aqueous drainage > ^IOP!

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4
Q

Clinical presentation of acute angle closure glaumcoma?

A

Onset occurs over hours-days.

  • Severe painful eye
  • Blurred vision/ coloured haloes around lights
  • Red eye
  • Pupil fixed + dilated (due to axonal death)
  • Hard Globe upon palpation
  • Systemic: malaise, N&V
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5
Q

Management of acute angle closure glaucoma?

A
  1. Urgent referral to opththalmology!!!!
  2. Avoid eye patches/ dark rooms- pupillary dilation will worsen angle closure.
  3. Triad of treatment
  4. Definitive: Peripheral Iridectomy- once IOP is controlled, involves removing iris segment to allow aqueous flow.
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6
Q

What is the triad of treatment in acute angle closure glaucoma?

A
  1. TOP B-blockers (timolol): suppresses aqueous humour production
  2. TOP Pilocarpine: miosis (constriction)- opens closed drainage angle. (Phenylephrine if lens replacement)
  3. IV Acetazolamide: for aqueous formation.

May also use steroids (pred)

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7
Q

Complications of acute angle closure glaucoma?

A

Visual loss

Central retinal artery/vein occlusion

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8
Q

Pathophysiology behind Cataracts? (opaque protein deposits in lens)

A
  • Lens capsule is elastic (collagen), epithelium (regulates homeostasis + lays down new fibres), fibres= bulk of lens!
  • Transparency maintained by structure of lens proteins
  • Disruption of crystalin fibres > protein aggregation
  • Age > accumulation to yellow-brown pigment in lens.
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9
Q

Presentation of cataracts?

A

Onset is gradual

  • Blurred vision > loss of vision (painless)
  • Loss of acuity, failure to recognise faces, trouble with nocturnal vision.
  • Dazzle/glare
  • Biplopia
  • Haloes/ opacity
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10
Q

What can be seen in fundoscopy/slit lamp whilst investigating cataracts?

A
  • Red light reflex: present if early, absent if late.

- Lens appears brown or white if bright light shone.

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11
Q

Different types of cataracts seen and their presentations on fundoscopy?

A
  • Nuclear cataracts (old age): refractive index variation.
  • Cortical cataracts: spoke-like wedge shape, milk effect on acuity.
  • Posterior subcapsular cataract: classic glare from sunlight/lights whilst driving at night, fast progression.
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12
Q

What are some types of management in cataracts?

A
  1. Conservative: mydriatic drops/ sunglasses
  2. Surgery:
    - Ocular biometry (pre-op), measure curvature of cornea + length of the eye to determine lens size.
    - Phaecoemulsion + intra-ocular lens implant

If congenital, must act within 4wks!

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13
Q

Prophylaxis of cataracts?

A
  • Sunglasses
  • Oxidative stress (anti-oxidants such as vit C + caffeine)
  • Stop smoking
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14
Q

What is a complication of cataracts? And what are the red flags for this?

A

Posterior sub-capsular cataracts! (progress faster)

  • Glare (from bright light)
  • Subcapsular opacity deep to lens capsule
  • Dot opacity

More common in diabetics/steroids

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15
Q

How does a corneal ulcer (aka ulcerative keratitis) develop?

A

Inflammation/infection of cornea > disruption of epithelial layer > ulcer.

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16
Q

What are some causes of corneal ulcers?

A
Bacterial
Herpetic (dendritic appearance)
Fungal (candida, aspegillus)
Protozoal (acanthamoeba)
Vasculitis (RA)
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17
Q

What are some risk factors for corneal ulcers?

A

Contact lenses
Trichiasis (abnormally positioned eye-lash can abrade cornea)
Ectropion (droopy lower eye lid > dry eye)
Steroid eye drops

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18
Q

Clinical presentation of corneal ulcer?

A
  • V painful eye, causes a squint
  • Red eye
  • Tearing + watery
  • Red
  • Reduced visual acuity
  • Photophobia
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19
Q

Investigations to do for a corneal ulcer?

A
  1. Refer to opthalm (same day)
  2. HIV testing! (important!)
  3. Slit lamp with 1% Fluorescein (differentiate between keratinic + dendritic ulcers)
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20
Q

Management of corneal ulcers?

A
  1. Chloramphenicol eye drops (gram +ve)
  2. Oflaxacin (gram -ve)
  3. Cefuroxime drops with Gentamicin drops
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21
Q

Red flag in corneal ulcers?

A

Herpes simplex dendritic corneal ulcers !! (HSV1 commonly manifests with corneal ulcers)

  • Acute pain, photophobia, watering.
  • Can lead to blindness (rapid progression)
  • TOP Aciclovir eye ointment !!!
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22
Q

What is a Chazalion?

A

Meibomian cyst! (non-infective)
Blocked meibomian (tarsal) gland (normally secretes sebum to hydrate eye > granulomatous inflammation in eye lid.
Most common lid lump.

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23
Q

What is a Hordeolum?

A

Stye!! (infective)

a) Internal (rare): meibomian gland infected > abscess
b) External (common): acute infection of last follicle + associated sebaceous glands of Moll/ Zeis.

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24
Q

Clinical presentation of a Chalazion?

A
  • Gradually enlarging round firm lesion: upper (common) or lower eye lid.
  • Can be painful initially (mostly non-tender)
  • Blurred vision/astygmatism if it compresses cornea.
  • Drains through inner eye lid/ absorbed in 2-8wks
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25
Q

Clinical presentation of Hordeolum?

A
  • Tender swelling, gradually enlarges.
  • Yellow swelling at base of eye lash (external hord)
  • Discharges anteriorly/posteriorly eventually
  • May develop rigors/fever
26
Q

Management of a Chazalion?

A
  1. Warm compress (twice daily) + massage lids
  2. Resection under LA
  3. Triamcinolone injection
  4. If persistent use Abx trial: Doxycycline
27
Q

Management of a Hordeum?

A

Antibiotics (TOP Choramphenicol or Doxycycline)

+ Curetting if necessary

28
Q

What causes conjunctivitis?

A

Infectious: viral (adenovirus 80%), or bacterial (staph)

Non-infectious: allergic (15-40% of all), mechanical/irritative/toxic, immune-mediated.

29
Q

Clinical presentation of conjunctivitis?

A
  • Red eye (generalised, often B/L)
  • Irritation, grittiness, discomfort
  • Discharge (watery (serous= viral), mucoid/string (allergic), sticky/purulent (bacterial)

Altered visual acuity/ intense pain- suggests alternative diagnosis.

30
Q

How do you investigate conjunctivitis?

A
  1. Examination of external eye + conjunctiva
  2. Ophthalmoscope:
    - dilated vessels
    - chemosis (conjunctival oedema)
    - Follicles (typically viral/bacterial/toxins)
    - Papillae (typically allergic immune response- cobblestone appearance of flattened nodules)
31
Q

Management of conjunctivitis:

1) Viral

A

1) Self limiting 1-2wks. Sx relief: TOP artificial tears + TOP anti-histamines e.g. Emedastine or olapatadine.

TOP antivirals do not work!

32
Q

Management of conjunctivitis:

2) Bacterial

A

Self-limiting 1-2wks

TOP Chloramphenicol, or Fusidic aid drops

33
Q

Management of conjunctivitis:

3) Allergic?

A

a) Cold press
b) TOP anti-histamines e.g. Emedastine or olopatadine
c) Sodium Cromoglicate + steroid drops

34
Q

What are signs of abrasion from a foreign body?

A

Conjunctival or ciliary injection (red), epithelial defects that stain with fluorescein.

35
Q

Foreign Body in Eye! RED FLAGS?

A
  • Evidence of open globe injury? (Distorted globe, leaking humour, subconjunctival haemorrhage) REFER immediately!
  • Evidence of deep eyelid laceration
  • Hyphaema (fluid level), irregular pupil, ^IOP (FP in anterior chamber)
36
Q

Management of an abrasion?

A

Abx: TOP Chloramphenicol (1st line)
Or Fusidic acid if pregnant.

Re-evaluate in 24hrs

37
Q

Management of a corneal foreign body/ penetrating corneal injury?

A
FB: remove under TOP anaesthetic. Irrigate eye with water.
Penetrating: 
-DO NOT TOUCH/ manipulate/ pad eye
-Give rigid eye shield to protect eye
-REFER IMMEDIATELY
-? tetanus shot
38
Q

What gene is Acute Anterior Uveitis associated with?

A

HLA-B27

(therefore associated with Anky Spond, reactive arthritis, UC/CD, Behcet’s dis.

39
Q

What is the classical presentation of Acute Anterior Uveitis?

A
  • Acute onset hours-days
  • Pain, red eye, blurred vision, photophobia
  • Pupil appears small (initially due to iris spasm), then becomes irregular + dilates due to adhesions.
  • This causes painful consensual reaction (constriction hurts)
  • May see Hypopyon (puss in anterior chamber)
40
Q

How do you investigate for Acute Anterior Uveitis?

A

Slit lamp!! (Diagnostic!)
-Leukocytes visible in anterior chamber
(no cells?- consider posterior uveitis)

41
Q

Management of Acute Anterior Uveitis?

A
  • REFER asap!
  • Cycloplegics to dilate pupil + relieve pain/ photophobia. + prevent formation of adhesions: TOP Atropine, cyclopentolate.
  • Steroid eye drops to reduce inflam: Prednisolone.
42
Q

Explain the terminology of the following (found in hypertensive retinopathy)

  • Tortuous vessels
  • Silver/Copper wiring
  • AV nipping
  • Cotton wool spots
  • Flame haemorrhage
  • Papilloedema
A
  • Tortuous vessels: dilated, abnormal path/shape
  • Silver/Copper wiring: shiny walls of blood vessels
  • AV nipping: narrowing where arteries cross veins
  • Cotton wool spots: fluffy areas indicating retinal infarction.
  • Flame haemorrhage: how a haemorrhage appears on a retina
  • Papilloedema: optic disc swelling from ^ICP
43
Q

What does the different grading mean in HTN Retinopathy?

A
  1. Arteriole narrowing or tortuosity and ^light reflex i.e. silver/copper wiring
  2. Arteriovenous (AV) nipping
  3. Cotton-wool exudate + Flame/Blot haemorrhages
  4. Papilloedema
44
Q

What does non-proliferative Diabetic Retinopathy look like ?

A

(Mild/moderate/severe depending on degree of ischaemia)
Signs: micro-aneurysms (seen as dots), haemorrhages (flame/blot), hard exudate (yellow patch)

Severe signs of ischaemia: soft exudate (cotton wool), large blot haemorrhages.

45
Q

What does proliferative Diabetic Retinopathy look like?

A

Fine new vessels appear (neovascularisation) on optic disc, retina + causes vitreous haemorrhage.

46
Q

What does maculopathy look like (in diabetic retinipathy)?

A

Leakage from vessels close to macula causes oedema, and then reduced acuity.

47
Q

Grading of Diabetic Retinopathy?

A
  1. Mild NPDR: 1 microaneurysm
  2. Moderate NPDR: >1 microaneurysm, hard exudate, cotton wool, dot/blot haemorrhage.
  3. Severe NPDR: more than moderate basically. More intra-retinal microvascular abnormalities.
  4. Proliferative DR (common in t1DM, 50% blind in 5yrs)
  5. Maculopathy (common t2DM)
48
Q

Symptoms/signs of Posterior Vitreous Detachment?

A
  • Flashes of light (photopsia)- in peripheral field of vision.
  • FLoaters, often on temporal side of central vision
49
Q

Symptoms/signs of retinal detachment?

A
  • Dense shadow (starts peripherally, goes towards central vision)
  • A veil/curtain over field of vision
  • Straigh lines appear curves
  • Central visual loss
50
Q

Symptoms/signs of vitreous haemorrhage?

A
  • Large bleeds cause sudden visual loss

- Small bleeds: floaters

51
Q

What are some retinal signs of papilloedema?

A
  • Venous engorgement (1st sign)
  • Blurring of optic disc contour/margin
  • Elevation of optic disc
  • Loss of Optic Cup
  • Paton’s lines: concentric lines cascading from optic disc
52
Q

Associated symptoms of papilloedema?

A
  • Severe throbbing headache (^ICP)
  • N^V (projectile)
  • Pupils will be normally equal + reactive to light!
53
Q

What is an Entropion?

A

Inversion of eyelid margin.

Caused by involution, secondary to ocular irritation.

54
Q

What is a common differential of entropion?

A

Trichiasis (misdirection of eyelashes)

55
Q

Management of Entropion?

A
  1. Lubricating eye drops
  2. Botox injections
  3. Surgical correction
56
Q

What is Ectropion? And what are some causes?

A
Eversion of eyelid margin.
Causes:
-Involuted (age-related)
-Paralytic (CNVII palsy)
-Mechanical (tumour= displacement)
-Congenital
57
Q

What eye condition is MS associated with?

And how does this present?

A

Optic neuritis!! (often unilateral)

  • Decreased visual acuity, progressive blurred vision, pain worse with movement, reduced colour vision.
  • Relevant Afferent Pupillary Defect (KEY!!)
  • Papilloedema
58
Q

What is the most common cause of persistent watery eye in infants?

A

Nasolacrimal duct obstruction.

teach lacrimal duct massage to parents, sx resolve in ~1year

59
Q

What is the most common cause of blindness in the UK?

A

Age Related Macular Degeneration (ARMD)

60
Q

What is the presentation of ARMD?

A
  • Degeneration of central retina (macula)
  • Dry: characterised by Drusen (yellow spots in Bruch’s membrane)
  • Wet (severe + rapid): choroidal neovasc, leakage of serous fluid/blood.
61
Q

What is the key symptom of Primary Open Angle Glaucoma?

A

Optic neuropathy, leading to reduced peripheral visual field!
=Tunnel vision!!

62
Q

What is 1st line in the management of Primary Open Angle Glaucoma?

A

Lantoprost (prostaglandin analogue)