Opthalmology Flashcards

1
Q

Pathophysiology of acute angle closure glaucoma?

A

IOP secondary to an impairment of aqueous outflow

hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age

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2
Q

Features of acute angle closure glaucoma?

A

severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain

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3
Q

Management of acvute angle glaucoma?

A

Combination of eye drops, for example:

1.Direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
2. Beta-blocker (e.g. timolol, decreases aqueous humour production)
3. Alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)

Plus:
Intravenous Azetazolamide

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4
Q

WHat is definitive management of acute angle closure glaucoma?

A

laser peripheral iridotomy
creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle

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5
Q

Most common cause of blindness in the UK?

A

Age related malcula degenration

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6
Q

Risk factors of age regulated macular degeneration?

A

Age
Smoke
Family history

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7
Q

What are the two forms of age related macular degeneration

A

Dry form - characterised by drusen - yellow round spots in Bruch’s membrane

Wet form - exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision

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8
Q

Presentation of ARMD?

A

reduction in visual acuity, particularly for near field object

difficulties in dark adaptation - poor night vision
fluctuations in visual disturbance
suffer from photopsia, (a perception of flickering or flashing lights)

distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen

wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.

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9
Q

Investigation of choice for ARMD?

A

Initial: slit-lamp microscopy is the initial investigation of choice

If postivie: fluorescein angiography is utilised if neovascular ARMD is suspected - guides anti VEGF

ocular coherence tomography is used to visualise the retina in three dimensions

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10
Q

What guides anti- VEGF in ARMD?

A

fluorescein angiography

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11
Q

Management of dry ARMD?

A

combination of zinc with anti-oxidant vitamins A,C and E

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12
Q

Management of wet ARMD?

A

anti-VEGF agents can limit progression of wet ARMD

anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,.

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13
Q

What are angiod retinal streaks?

A

irregular dark red streaks radiating from the optic nerve head.

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14
Q

Causes of angiod retinal streaks?

A

pseudoxanthoma elasticum
Ehler-Danlos syndrome
Paget’s disease
sickle-cell anaemia
acromegaly

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15
Q

HLA association with anterior uvetitis?

A

HLA B27

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16
Q

Factures of anterior uveitis?

A

acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired

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17
Q

Associated conditiosn of anterior uveitis?

A

ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen

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18
Q

Management of anterior uveitis?

A
  1. urgent review by ophthalmology
  2. cycloplegics (dilates the pupil which helps to relieve 3. pain and photophobia) e.g. Atropine, cyclopentolate
    steroid eye drops
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19
Q

What is an argle robertson pupile?

A

Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

small, irregular pupils
no response to light but there is a response to accommodate

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20
Q

Risk factors of argyle robertson pupil?

A

Diabetes
Syphilus

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21
Q

Pathophysiology in blepharitis?

A

meibomian gland dysfunction (common, posterior blepharitis)

seborrhoeic dermatitis/staphylococcal infection

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22
Q

Features of blepharitis?

A

symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur

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23
Q

Management of belpharitis?

A

Hot compresses

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24
Q

Features of central retinal artery occlusion?

A

sudden, painless unilateral visual loss
relative afferent pupillary defect
‘cherry red’ spot on a pale retina

Either from thromboembolism or arteritis - temporal arteritis

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25
Q

Risk factors for central retinal vein occlusion?

A

increasing age
hypertension
cardiovascular disease
glaucoma
polycythaemia

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26
Q

Features of central retinal vein occlusion@?

A

sudden, painless reduction or loss of visual acuity, usually unilaterally
fundoscopy
widespread hyperaemia
severe retinal haemorrhages - ‘stormy sunset’

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27
Q

Management of central retinal vein occlusion

A

the majority of patients are managed conservatively

indications for treatment in patients with CRVO include:

macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents

retinal neovascularization - laser photocoagulation

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28
Q

Pathophysiology of diabetic retinopathy?

A

Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls.

Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy.

formation of microaneurysms.

Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia

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29
Q

Features of mild diabetic retinopathy?
(non-proliferative)

A

1 or more microaneurysm

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30
Q

Features of moderate diabetic retinopathy?
(non-proliferative)

A

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

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31
Q

Features of severe diabetic retinopathy?
(Non-proliferative)

A

blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant

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32
Q

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, 50% blind in 5 years

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33
Q

Treatment of maculopathy in diabetic retinopathy?

A

intravitreal vascular endothelial growth factor (VEGF) inhibitors

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34
Q

Management of proliferative diabetic retinopathy?

A

panretinal laser photocoagulation
intravitreal VEGF inhibitors
ranibizumab

severe or vitreous haemorrhage: vitreoretinal surgery

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35
Q

Most common cause of corneal dendritic ulcer?

A

Herpes simplex

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36
Q

Features of herpes simplex keratitis?

A

red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer

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37
Q

Features of herpes simplex keratitis?

A

red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer

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38
Q

Management of herpes simplex keratitis?

A

immediate referral to an ophthalmologist
topical aciclovir

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39
Q

WHat is herpes zoster ophthalmicus?

A

Reactivation of herpez zoster in ophthalmic division of trigeminal nerve

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40
Q

Features of herpes zoster ophthalmicus?

A

vesicular rash around the eye, which may or may not involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

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41
Q

Management of herpes zoster opthalmicus?

A

oral antiviral treatment for 7-10 days
ideally started within 72 hours
intravenous antivirals may be given for very severe infection or if the patient is immunocompromised
topical antiviral treatment is not given in HZO

topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review

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42
Q

Complications of herpes zoster ophthalmicus?

A

ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia

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43
Q

What is Holmes addie pupil?

A

benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.

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44
Q

Feautres of holms addie pupil

A

unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light

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45
Q

What is holms addie syndrome?

A

association of Holmes-Adie pupil with absent ankle/knee reflexes

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46
Q

Features of horner’s syndrome?

A

miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)

47
Q

Horners + Heterochromia?

A

congenital Horner’s

48
Q

What are the three areas a lesion may be to cause horners?

A

Central
Preganglionic
Post ganglionic

49
Q

Features of central hroners and causes?

A

Anhidrosis of face, arms trunk

Stroke
Syringomyelia
Multiple sclerosis

50
Q

Features of preganglionic lesion horners/

A

Anhidrosis of face

Pancoast’s tumour
Thyroidectomy
Trauma
Cervical rib

51
Q

Features of post ganglionic lesions horners?

A

Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache

52
Q

Features of grade 1 hypertensive retinopathy?

A

Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring

53
Q

Features of grade 2 hypertensive retinopathy?

A

Arteriovenous nipping

54
Q

Features of grade 3 hypertensive retinopathy?

A

Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’

55
Q

Features of grade 4 hypertensive retinopathy?

A

Papilloedema

56
Q

What is keratitis?

A

Inflammation of cornea - sight ending possibly

red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen

57
Q

Causes of keratitis?

A

Bacterial
- typically Staphylococcus aureus
- Pseudomonas aeruginosa is seen in contact lens wearers

Fungal
- amoebic
- acanthamoebic keratitis

parasitic: onchocercal keratitis (‘river blindness’)

58
Q

Management of keratitis?

A

stop using contact lens until the symptoms have fully resolved
topical antibiotics
typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate

59
Q

What is dacrocystitis?

A

infection of the lacrimal sac

watering eye (epiphora)
swelling and erythema at the inner canthus of the eye

60
Q

Causes of mydriasis ( dilated) eye?

A

third nerve palsy
Holmes-Adie pupil
traumatic iridoplegia
phaeochromocytoma
congenital

61
Q

Drug causes of mydriasis?

A

topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants

62
Q

Causes of optic atrophy?

A

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

63
Q

Causes of congenital optic atrophy?

A

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)

64
Q

Causes of optic neuritis?

A

multiple sclerosis: the commonest associated disease
diabetes
syphilis

65
Q

Features of optic neuritis?

A

unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma

66
Q

Best investigation of optic nueirits?

A

MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases

67
Q

Management of optic neuritis?

A

high-dose steroids
recovery usually takes 4-6 weeks

68
Q

Management of optic neuritis?

A

high-dose steroids
recovery usually takes 4-6 weeks

69
Q

What is orbital cellulitis?

A

infection affecting the fat and muscles posterior to the orbital septum,

70
Q

Presentation of orbital cellulitls?

A

Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis
Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)

71
Q

Most common bacteria for orbital cellulitis?

A

Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.

72
Q

Papilloedema findings on fundoscopy?

A

venous engorgement: usually the first sign
loss of venous pulsation: although many normal patients do not have normal pulsation
blurring of the optic disc margin
elevation of optic disc
loss of the optic cup
Paton’s lines: concentric/radial retinal lines cascading from the optic disc

73
Q

Causes of papilloedema?

A

space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia

74
Q

Rare causes of papilloedema?

A

hypoparathyroidism and hypocalcaemia
vitamin A toxicity

75
Q

Feautres of posterior vitreal detachment ?

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
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)

76
Q

Finds of posterior vitreal detachment on fundoscopy?

A

Weiss ring on ophthalmoscopy

77
Q

Management of posterior vitreal detachment?

A

Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.

78
Q

Mechanism of prostaglandin analogues in glaucoma?

A

Increases uveoscleral outflow

79
Q

Mechanism of beta blockers in glaucoma?

A

Reduces aqueous production

80
Q

Mechanism of Sympathomimetics n glaucoma?

A

brimonidine, an alpha2-adrenoceptor agonist)

Reduces aqueous production and increases outflow

81
Q

Mechanism of carbonic anhydrase inhibitors?

A

Dorzolamide

Reduces aqueous production

82
Q

Mechanism of miotics in glaucoma?

A

Increases uveoscleral outflow

83
Q

Red eye + small fixed pupil?

A

acute angle closure

severe pain (may be ocular or headache)
decreased visual acuity, patient sees haloes
semi-dilated pupil
hazy cornea

84
Q

Red eye + small, fixed oval pupil, ciliary flush?

A

Anterior uveitis

acute onset
pain
blurred vision and photophobia
small, fixed oval pupil, ciliary flush

85
Q

Scleritis?

A

severe pain (may be worse on movement) and tenderness
may be underlying autoimmune disease e.g. rheumatoid arthritis

86
Q

Endopthalmoous

A

Endophthalmitis
typically red eye, pain and visual loss following intraocular surgery

87
Q

What is marcus gunn pupil?

A

Relative afferent pupillary defect

88
Q

Features of relative afferent pupillary defect?

A

the affected and normal eye appears to dilate when light is shone on the affected

89
Q

Causes of relative afferent pupillary defectr?

A

retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis

90
Q

Pathway of pupillary light reflex?

A

afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve

91
Q

Features of retinitis pigmentosa?

A

night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium

92
Q

Associated diseases of retinitis pigmentosa?

A

Kearns-Sayre syndrome
Alport’s syndrome

93
Q

Ocular manifestations of rheumatoid arthritis?

A

keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis

94
Q

What visual problem does chloroquine cause?

A

Retinopathy

95
Q

What visual problem do steroids cause?

A

Cataracts

96
Q

Management of amarouosis fugax?

A

Asprin 300 mg

97
Q

Fundoscopy of central retinal vein occlusion?

A

severe retinal haemorrhages are usually seen on fundoscopy

98
Q

Fundoscopy of central retinal artery occlusion?

A

features include afferent pupillary defect, ‘cherry red’ spot on a pale retina

99
Q

Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision

A

Posterior vitreal detachment

100
Q

Dense shadow that starts peripherally progresses towards the central vision

A

Retinal detachment

101
Q

Tunnel vision causes?

A

papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria

102
Q

Anhidrosis horners?

A

head, arm, trunk = central lesion: stroke, syringomyelia
just face = pre-ganglionic lesion: Pancoast’s, cervical rib
absent = post-ganglionic lesion: carotid artery

103
Q

Episcleritis painful?

A

No
Associated with RA

104
Q

Macular degenration biggest risk facotr?

A

smoking

105
Q

Central retinal vein loss, painful?

A

No

106
Q

What are the major risks for orbital cellulitis?

A

Cavernous sinus thrombosis
Intracranial spread

107
Q

First line drop in glaucoma for asthmatics?

A

Prostaglandins

108
Q

black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium

A

Retinitis pigmentosa

109
Q

What is a postive relative afferent pupillary defect?

A

relative afferent pupillary defect is when the affected and normal eye appears to dilate when light is shone on the affected eye

110
Q

Durgs that increase acute angle closure glaucoma?

A

Anti muscarinics
TCI’s

111
Q

Treatment of herpes zoster ophtalmicus?

A

Oral aciclovir

112
Q

Enlarging dark spot

A

Vitreous haemorrhage

113
Q

Dense shadow

A

Retinal detachment