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SPM > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

normal eye pressure

A

11-21mmHg

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2
Q

what happens in posterior vitreous detachment

A

caused by natural changes to the vitreous gel with age - it shrinks and develops pockets of liquefaction (think gelatin dessert)

at some stage it may peel away from retina

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3
Q

symptoms of posterior vitreous detachment

A

photopsia (flashes of light) in the peripheral field of vision

sudden dramatic increase in floaters - often on the temporal side of the central vision

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4
Q

what is PVD more common in

A

myopia - eye is too long

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5
Q

retinal tear

A

retinal develops small gaps - can cause retinal detachment in rare cases. caused by ageing or injury

symptoms are mild - may see black spots or floaters and cause distorted vision

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6
Q

retinal detachment symptoms

A

floaters, flashes of light
loss of central vision - dense shadow that starts peripherally progresses towards the central vision
straight lines appear curved

painless

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7
Q

treatment of retinal detachment

A

not always required unless there is tears – symptoms gradually improve over 6 months

cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall of the areas of detachment so that it does not spread

or scleral buckle surgery or pneumatic retinoplexy or vitrectomy

85 percent of cases will be successfully treated with one operation with the remaining 15 percent requiring 2 or more operations. After treatment patients gradually regain their vision over a period of a few weeks

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8
Q

vitreous haemorrhage

A

o Leakage of blood into the areas in and around the vitreous humor

Large bleeds cause sudden visual loss

Moderate bleeds may be described as numerous dark spots

Small bleeds may cause floaters

o Causes include diabetic retinopathy, trauma, retinal tear or detachment, posterior vitreous detachment
o Treatment – advised to rest with head elevated, can put patch over eye to limit movement, stop blood thinners, retinal tears should be closed by laser treatment or cryotherapy and detached retinas should be reattached

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9
Q

causes of transient visual loss

A

unilateral

  • amourosis fugax (can be one or both). embolic, haeodynamic, ocular, neurologic, idiopathic
  • giant cell arteritis can cause double vision or partial loss of vision (treat with high dose prednisolone)

bilateral

  • TIAs
  • migraine
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10
Q

causes of double vision

A

binocular - strabismus, nerves (MS, GB, diabetes), stoke, muscle (MG, Grave’s)

monocular - cataract

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11
Q

primary angle closure suspect (PACS)

A

here goinoscopy shows some closure but the person has normal IOP and no signs of glaucoma

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12
Q

pressure in acute angle closure glaucoma

A

ophthalmic emergency

sudden risk of pressure to >50mmHg

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13
Q

risk factors for acute angle closure glaucoma

A 
female
asian
hyermetropia because of shallower anterior chambers (smaller eye)
FHx
age

the attack is more likely to occur under reduced light conditions when the pupil is dilated

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14
Q

acute angle closure glaucoma presentation

A

sudden onset of a red painful eye and blurred vision
and patients become unwell with N+V

the cornea is hazy and the pupil is semi-dilated

gets halos around lights (rainbow-coloured)

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15
Q

investigations for acute angle closure glaucoma

A

goinoscopy -definitive test - trabecular meshwork won’t be visible

slit lamp exam - will see shallow anterior chamber and large optic cup (NB goinoscopy is usually performed at the slit lamp)

automatic static perimetry using Humphrey’s visual field test to check for the amount of glaucomatous visual field loss during initial diagnosis

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16
Q

treatment of acute angle closure glaucoma

A

URGENT
lie flat with their face up and head not supported by pillows

IV acetazolamide 500mg to reduce IOP (CA inhibitor) and pilocarpine 4% drops to constrict the pupil and to prevent iris adhesion to trabecular meshwork

other topical drops like beta blockers (timolol) and prostaglandin analogues can also be instilled if available

DEFINITIVE TREATMENT = laser iridotomy after initial corneal oedema resolves

the unaffected eye is also usually treated

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17
Q

most common type of glaucoma

A

primary open angle glaucoma

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18
Q

risk factors for primary open angle glaucoma

A 
FHx
high myopia (short-sightedness)
DM
age (subtle changes in structure of trab mw occur)
2x more common in black 
steroids 
HTN
CV disease

reduced drainage of aqueous humour from the anterior chamber

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19
Q

vision loss in primary open angle glaucoma

A

peripheral occurs first

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20
Q

presentation of primary open angle glaucoma

A

usually asymptomatic and insidious in onset - e.g. picked up by routine eye exam
usually affects both eyes
visual loss only noticed when advanced - peripheral

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21
Q

investigations for primary open angle glaucoma

A

tonometry - Goldmann tonometry to determine IOP

direct ophthalmoscopy to view cup to disc ratio

indirect opthalmoscopy can also show cup to disc ratio

slip lamp exam is most frequent method used - IOP can be measured and drainage angle assessed

visual field testing should be done on all - scotoma with either an elevated IOP or enlarged cup to disc ratio have high sensitivity and specificity

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22
Q

primary open angle glaucoma treatment

A

topical prostaglandin analogues e.g. latanoprost or topical beta blocker like timolol

2nd line treatments include CA inhibitors, alpha 2 adrenergic agonsits or a combination

if eye drops fail, surgery can be done like laser trabeculoplastyto improve drainage

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23
Q

PAOG blindess

A

deveops in 5-10%

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24
Q

pathophysiology of diabetic retinopathy

A

hyperglycaemia damages retinal pericytes which results in weakening of cap walls and increased blood flow leading to microaneurysms at areas of weakness

it also means vessels are more leaky to proteins and lipids leak out forming hard exudates

= pre-proliferative stage (typically 15 years after diagnosis and can last a few years before becoming proliferative)

at proliferative stage, there is vascular prolideration and most patients will have at least blurry vision or floaters

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25
Q

vision loss in diabetic retinopathy

A

gradual loss of vision - central - due to macula oedema

or can get sudden loss of vision due to vitreous haemorrhage

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26
Q

cotton wool spots

A

represent the arrest of axoplasmic material at the margin of a microvascular infarct - thought to represent nerve fiber layer infarct

they are predictive to the progression to PDR

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27
Q

eye palsies

A 
CN3 = down and out
CN4 = down and in
CN6 = in
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28
Q

investigations for diabetic eye disease

A

ocular movements to detect any ocular motor palsies
check red reflex due to increased risk of cataracts
visual acuity
photographs at fundus at baseline
optical coherence tomography scanning to show macular oedema or retinal thickening
fluorescein angiography to identify macular leakage

B scan US to identify retinal detachment with vitreous haemorrhage

29
Q

grading of diabetic retinopathy

A 
R0 = no retinopathy
R1 = background
R2 = pre-proliferative 
R3 = proliferative (A = active, S - stable, P - previous photocoagulation laser treatment)
M0 = no maculopathy
M1 = maculoapthy present
30
Q

treatment for clinically signification macular oedema (CSMO)

A

intravitreal anti-VEGF +/- macular laser therapy

Anti-VEGF include ranibizumab and bevacizumab
macular laser is used to seal the blood vessels around the macular that are leaking and causing the oedema

31
Q

development of new blood vessels in diabetic retinopathy treatment

A

pan-retinal photocoagulation
where a laser is used to cauterise ocular blood vessels

is aimed at preventing serious complications like vitreous haemorrhage and retinal detachment

32
Q

severe proliferative diabetic retinopathy treatmnet

A

vitrectomy - some or all of the vitreous gel is removed in order to clear the blood from the vitreous humour - is used if bleeding is recurrent and §preventing pan retinal photocoagulation laser therapy

33
Q

classification of cataracts

A

nuclear sclerotic - commonest

cortical

posterior or anterior sub-capsular

  • posterior is seen frequently due to drugs e.g. topical corticosteroids or metabolic cataracts
  • anterior is seen in blunt traumatic injuries
34
Q

presentation of cataracts

A

gradual blurred/cloudy/misty vision and glare

in nuclear cataracts, can get washed-out colour vision

35
Q

investigations in cataracts

A

test visual acuity
dilated fundus exam with an opthalmoscope - fundus and optic nerve should be normal. will see reduced red relfex and opacification of lens
measure IOP - should be normal - gold standard is via Goldmann applanation tonometry
slit lamp exam of the anterior chamber will allow better visualisation of the cataract

36
Q

cataract surgery

A

done once person has functional visual impairment

done as a day case under LA
incision at the corneascleral junction approx 4mm
capsulorhexis - removal of the anterior lens capsule
high speed ultrasonic vibrating tip cuts nucleus into smaller fragments and aspirates them (phakoemulsification)
aspiration of soft lens matter
insertion of posterior chamber IOL (intraocular lens) into capsular bag

post operative treatment is with topical steroids and topical Abx

37
Q

complications of cataract surgery

A

rupture of posterior lens capsule causing vitreous loss - if this occurs before the lens nucleus is removed = dropped nucleus - will require another operation to remove it

endophthalmitis = 0.1% risk - commonest organismis staph epidermis

posterior capsular opacification - a healing response that can be corrected by laser treatment - is where the back of the lens becomes cloudy causing blurred vision

38
Q

what is age related macula degeneration

A

characterised by degeneration of retinal photoreceptors that results from the formation in drusen
usually bilateral
the drusen occur beneath the retinal pigment epithelium within Bruch’s membrane
drusen alters the permeability of Bruch’s membrane resulting in decreased nutrient delivery to RPE cells and secondary metabolic stress

39
Q

risk factors for AMD

A

smokers have a 2-3x increased risk
FHx
genetic factors

40
Q

symptoms of AMD

A

distortion is usually the first symptom - straight lines appear crooked or wavy

gradual loss of central vision - difficulty with reading + recognising faces

wet type: if associated with haemorrhage may have sudden deterioration

eventually severe central field loss but maintain peripheral vision

41
Q

AMD investigations

A

visual acuity - may be normal or reduced

fundoscopy + photography - may see drusen or pigmentary, haemorrhageic or atropic changes affecting the macula

slit lamp - same as above

Amsler grid - distortion (metamorphopsia)

optical corherence tomography - definitive test for confirming presence of subretinal and intraretinal fluid

fluorescein angiography if neovascular AMD is suspected

42
Q

management of AMD

A

slow progression by stopping smoking, eat heathily
consider registering as sight impaired
signpost to relevant organisations, sources of info
high-dose antioxidant and mineral supplementation like zinc

for neovascular AMD:

  • anti-VEGF like ranibizumab, afilbercept via intravitral injection (monthly for 3 months then variable times thereafter)
  • others (although not usually recommended) - laser photocoagulation or photodynamic therapy with verteprofin

an emerging treatment: implantable miniature telescope that focuses the central visual field onto areas of the retina not affected by AMD

43
Q

3 causes of painless red eye

A

CES
conjunctivitis
episcleritis
subconjunctival haemorrhage

and blepharitis - but this causes more of a red eyelid rather than eye

44
Q

hazy cornea, haloes

A

acute angle closure glaucoma

45
Q

ciliary flush

A

anterior uveitis
corneal abscess
contact lens related red eye

46
Q

cause of blepharitis

A 
anterior = inflammation of the base of the eyelashes. can be caused by bacteria (usually staphylococci) or seborrhoeic dermatitis
posterior = inflammation of the meibomian glands

can also be associated with acne rosace

47
Q

blepharitis presentation

A

minimal red eye
burning, itching, erythema and crusting of eyelids

no pain, no photophobia, no visual loss

chalazions (cysts in the eyelid due to inflammation of blocked meibomian glands)

48
Q

management of blepharitis

A

Eyelid hygiene measures and warm compresses

Consideration of topical antibiotics (such as chloramphenicol) if hygiene measures have failure

49
Q

stye (hordeolum) vs chalazion

A

stye = bacterial infection either at the root of the eyelash follicle or in the oil gland of the lids

chalazion = blocked oil gland

chalazion are painless

50
Q

treatment of entropion

A

Topical antibiotic to prevent infection. Taping down lower lid (temporary measure). Long term correction with surgical procedure under LA

51
Q

treatment of ectropion

A

With lateral tarsal strip operation and lubricating eye drops

52
Q

3 types of conjunctivitis

A

viral - adenovrius, herpes simplex, EBV, VZV, enterovirus
bacterial - pneumonococcus, s aureus, haemophilius influenae, moraxella catarrhalis
allergic - can be seasonal (hay fever associated) or non-seasonal (dust mites, pets)

53
Q

hyperacute conjunctivitis

A

is a rapidly developing severe conjunctivitis typically caused by infection with Neisseria gonorrhea

54
Q

symptoms of conjunctivitis

A

discomfort that may be described as a foreign body or burning sensation
watery or purulent discharge
tender, pre-auricular lymphadenopathy more common in viral
unilateral in bacterial, bilateral in viral
itchiness more common in allergic
allergic might be more red around the eye

HSV conjunctivitis may have vesicular lesions on the eyelid

55
Q

management of viral conjunctivitis

A

o Usually resolves within 7 days
o Provision of patient information
o Advise self-care measures such as bathing/cleaning the eyelids, cool compresses, lubricating drops or artificial tears
o Avoid contact lenses
o Inform the person that it is contagious, and they should try to prevent spread of infection to their other eye and other people by
 Using separate towels, avoiding close contact (but do not have to exclude from school), wash hands frequently
o Consider discussion with/referral to ophthalmology is symptoms persist for more than 7-10 days after initiating treatment
o Consider swabbing for HSV if they re-attend

56
Q

management

A

o Advice the person that most cases are self-limiting and resolve within 5-7 days without treatment. + general hygiene measures by not sharing towels etc.
o Provision of patient information
o Advise self-care measures such as bathing/cleaning the eyelids, cool compresses, lubricating drops or artificial tears
o Avoid contact lenses
o If severe or circumstances that require rapid resolution, then treat with topical antibiotics
o A delayed strategy may be appropriate – advise the person to initiate them if symptoms have not resolved within 3 days
 Chloramphenicol 0.5% drops
o Explain red flags for urgent review e.g. reduced visual acuity or photophobia §

57
Q

antibiotic for bacterial conjunctivitis

A

chloramphenicol

58
Q

red flags with conjunctivitis for need of urgent opthalmological assessment

A
  • Reduced visual acuity
  • Infection with a herpes virus – requires treatment with oral antivirals
  • Marked eye pain, headache or photophobia – always consider serious systemic conditions such as meningitis
  • If you suspect gonococcal or chlamydial conjunctivitis
59
Q

gonococcal vs chamyldial neonatal conjunctivitis

A

gonococcal in 1st 5 days whereas C trachomatis 3 days – 2 weeks

60
Q

management of subconjunctival haemorrhage

A

reassure that it will clear in 2-3 weeks

measure the person’s BP and if raised, manage appropriately

check the person’s INR if they are taking warfarin and manage accordingly

61
Q

keratitis define

A

= inflammation of the cornea

an ocular emergency (bacterial)

62
Q

causes of keratitis

A

viral (HSV, herpes zoster)
contact lens-associated infection
blepharitis
bacterial (pseudomonas aeruoginosa or staph aureua)

less common - fungal (aspergillus fumigatus or candida albicans)

predisposing factor = compromised corneal epithelium e.g. via corneal abrasions, contact lenses, topical steroids, corneal anasethesia

63
Q

presentation of keratisis

A 
red eye (conjunctival injection)
severe pain - gritty or foreign body
photophobia
decreased VA
discharge

bacterial keratitsi- corneal ulcer (white and fluffy)

herpes simplex keratitis - branching dendritic ulcer with fluorescein

64
Q

investigations for keratitis

A

confirmed if a corneal lesion is seen on slit-lamp examination - an epithelial defect can easily be seen after staining the cornea with flueorescein

can measure visual acuity with a Snellen chart

corneal scraping for a culture / viral PCR

consider FBC - may indicate systemic infection or immune compromise

65
Q

treatment of keratitis

A

bacterial = topical broad spectrum Abx (ofloxacin) + pain relief + cautious use of topical steroids to reduce scarring (usually 48 hrs after initiation of Abx)

viral - topical gancicliovir or oral acyclovir

contact lens wearers are advised to discontinue wear

66
Q

foreign body management

A

Instill topical local anaesthetic and remove FB (+/- rust ring) with cotton wool bud or tip of 21G needle
Instill topical antibiotic and eye pad overnight
Topical antibiotic qds for 1/52 to prevent secondary bacterial infection

67
Q

corneal abrasion due to infection related to contract lens wear

A

acanthamoeba

or pseudomonas

68
Q

corenal abrasion/ulceration diagnosis

A

fluorescein stain - Fluorescein stains any exposed corneal stroma (yellow-orange) and basement membrane – it does not stain intact conjunctival or corneal epithelium
slit lamp
fundoscopic exam is often difficult as the pupil may be small and person photophobic

69
Q

colour of fluoroscein stain

A

uses an orange dye and a blue light – any problems will appear green under the blue light

SPM (9 decks)

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