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MRCP Opthalmology > Opthalmology > Flashcards

Opthalmology Flashcards

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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
Risk factors for central retinal vein occlusion?
increasing age hypertension cardiovascular disease glaucoma polycythaemia
26
Features of central retinal vein occlusion@?
sudden, painless reduction or loss of visual acuity, usually unilaterally fundoscopy widespread hyperaemia severe retinal haemorrhages - 'stormy sunset'
27
Management of central retinal vein occlusion
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
28
Pathophysiology of diabetic retinopathy?
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
29
Features of mild diabetic retinopathy? (non-proliferative)
1 or more microaneurysm
30
Features of moderate diabetic retinopathy? (non-proliferative)
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
31
Features of severe diabetic retinopathy? (Non-proliferative)
blot haemorrhages and microaneurysms in 4 quadrants venous beading in at least 2 quadrants IRMA in at least 1 quadrant
32
Features of proliferative diabetic retinopathy?
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
33
Treatment of maculopathy in diabetic retinopathy?
intravitreal vascular endothelial growth factor (VEGF) inhibitors
34
Management of proliferative diabetic retinopathy?
panretinal laser photocoagulation intravitreal VEGF inhibitors ranibizumab severe or vitreous haemorrhage: vitreoretinal surgery
35
Most common cause of corneal dendritic ulcer?
Herpes simplex
36
Features of herpes simplex keratitis?
red, painful eye photophobia epiphora visual acuity may be decreased fluorescein staining may show an epithelial ulcer
37
Features of herpes simplex keratitis?
red, painful eye photophobia epiphora visual acuity may be decreased fluorescein staining may show an epithelial ulcer
38
Management of herpes simplex keratitis?
immediate referral to an ophthalmologist topical aciclovir
39
WHat is herpes zoster ophthalmicus?
Reactivation of herpez zoster in ophthalmic division of trigeminal nerve
40
Features of herpes zoster ophthalmicus?
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
41
Management of herpes zoster opthalmicus?
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
42
Complications of herpes zoster ophthalmicus?
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis ptosis post-herpetic neuralgia
43
What is Holmes addie pupil?
benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.
44
Feautres of holms addie pupil
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
45
What is holms addie syndrome?
association of Holmes-Adie pupil with absent ankle/knee reflexes
46
Features of horner's syndrome?
miosis (small pupil) ptosis enophthalmos* (sunken eye) anhidrosis (loss of sweating one side)
47
Horners + Heterochromia?
congenital Horner's
48
What are the three areas a lesion may be to cause horners?
Central Preganglionic Post ganglionic
49
Features of central hroners and causes?
Anhidrosis of face, arms trunk Stroke Syringomyelia Multiple sclerosis
50
Features of preganglionic lesion horners/
Anhidrosis of face Pancoast's tumour Thyroidectomy Trauma Cervical rib
51
Features of post ganglionic lesions horners?
Carotid artery dissection Carotid aneurysm Cavernous sinus thrombosis Cluster headache
52
Features of grade 1 hypertensive retinopathy?
Arteriolar narrowing and tortuosity Increased light reflex - silver wiring
53
Features of grade 2 hypertensive retinopathy?
Arteriovenous nipping
54
Features of grade 3 hypertensive retinopathy?
Cotton-wool exudates Flame and blot haemorrhages These may collect around the fovea resulting in a 'macular star'
55
Features of grade 4 hypertensive retinopathy?
Papilloedema
56
What is keratitis?
Inflammation of cornea - sight ending possibly red eye: pain and erythema photophobia foreign body, gritty sensation hypopyon may be seen
57
Causes of keratitis?
Bacterial - typically Staphylococcus aureus - Pseudomonas aeruginosa is seen in contact lens wearers Fungal - amoebic - acanthamoebic keratitis parasitic: onchocercal keratitis ('river blindness')
58
Management of keratitis?
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
What is dacrocystitis?
infection of the lacrimal sac watering eye (epiphora) swelling and erythema at the inner canthus of the eye
60
Causes of mydriasis ( dilated) eye?
third nerve palsy Holmes-Adie pupil traumatic iridoplegia phaeochromocytoma congenital
61
Drug causes of mydriasis?
topical mydriatics: tropicamide, atropine sympathomimetic drugs: amphetamines, cocaine anticholinergic drugs: tricyclic antidepressants
62
Causes of optic atrophy?
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
Causes of congenital optic atrophy?
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
Causes of optic neuritis?
multiple sclerosis: the commonest associated disease diabetes syphilis
65
Features of optic neuritis?
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
Best investigation of optic nueirits?
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
67
Management of optic neuritis?
high-dose steroids recovery usually takes 4-6 weeks
68
Management of optic neuritis?
high-dose steroids recovery usually takes 4-6 weeks
69
What is orbital cellulitis?
infection affecting the fat and muscles posterior to the orbital septum,
70
Presentation of orbital cellulitls?
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
Most common bacteria for orbital cellulitis?
Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
72
Papilloedema findings on fundoscopy?
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
Causes of papilloedema?
space-occupying lesion: neoplastic, vascular malignant hypertension idiopathic intracranial hypertension hydrocephalus hypercapnia
74
Rare causes of papilloedema?
hypoparathyroidism and hypocalcaemia vitamin A toxicity
75
Feautres of posterior vitreal detachment ?
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
Finds of posterior vitreal detachment on fundoscopy?
Weiss ring on ophthalmoscopy
77
Management of posterior vitreal detachment?
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
Mechanism of prostaglandin analogues in glaucoma?
Increases uveoscleral outflow
79
Mechanism of beta blockers in glaucoma?
Reduces aqueous production
80
Mechanism of Sympathomimetics n glaucoma?
brimonidine, an alpha2-adrenoceptor agonist) Reduces aqueous production and increases outflow
81
Mechanism of carbonic anhydrase inhibitors?
Dorzolamide Reduces aqueous production
82
Mechanism of miotics in glaucoma?
Increases uveoscleral outflow
83
Red eye + small fixed pupil?
acute angle closure severe pain (may be ocular or headache) decreased visual acuity, patient sees haloes semi-dilated pupil hazy cornea
84
Red eye + small, fixed oval pupil, ciliary flush?
Anterior uveitis acute onset pain blurred vision and photophobia small, fixed oval pupil, ciliary flush
85
Scleritis?
severe pain (may be worse on movement) and tenderness may be underlying autoimmune disease e.g. rheumatoid arthritis
86
Endopthalmoous
Endophthalmitis typically red eye, pain and visual loss following intraocular surgery
87
What is marcus gunn pupil?
Relative afferent pupillary defect
88
Features of relative afferent pupillary defect?
the affected and normal eye appears to dilate when light is shone on the affected
89
Causes of relative afferent pupillary defectr?
retina: detachment optic nerve: optic neuritis e.g. multiple sclerosis
90
Pathway of pupillary light reflex?
afferent: retina → optic nerve → lateral geniculate body → midbrain efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
91
Features of retinitis pigmentosa?
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
Associated diseases of retinitis pigmentosa?
Kearns-Sayre syndrome Alport's syndrome
93
Ocular manifestations of rheumatoid arthritis?
keratoconjunctivitis sicca (most common) episcleritis (erythema) scleritis (erythema and pain) corneal ulceration keratitis
94
What visual problem does chloroquine cause?
Retinopathy
95
What visual problem do steroids cause?
Cataracts
96
Management of amarouosis fugax?
Asprin 300 mg
97
Fundoscopy of central retinal vein occlusion?
severe retinal haemorrhages are usually seen on fundoscopy
98
Fundoscopy of central retinal artery occlusion?
features include afferent pupillary defect, 'cherry red' spot on a pale retina
99
Flashes of light (photopsia) - in the peripheral field of vision Floaters, often on the temporal side of the central vision
Posterior vitreal detachment
100
Dense shadow that starts peripherally progresses towards the central vision
Retinal detachment
101
Tunnel vision causes?
papilloedema glaucoma retinitis pigmentosa choroidoretinitis optic atrophy secondary to tabes dorsalis hysteria
102
Anhidrosis horners?
head, arm, trunk = central lesion: stroke, syringomyelia just face = pre-ganglionic lesion: Pancoast's, cervical rib absent = post-ganglionic lesion: carotid artery
103
Episcleritis painful?
No Associated with RA
104
Macular degenration biggest risk facotr?
smoking
105
Central retinal vein loss, painful?
No
106
What are the major risks for orbital cellulitis?
Cavernous sinus thrombosis Intracranial spread
107
First line drop in glaucoma for asthmatics?
Prostaglandins
108
black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Retinitis pigmentosa
109
What is a postive relative afferent pupillary defect?
relative afferent pupillary defect is when the affected and normal eye appears to dilate when light is shone on the affected eye
110
Durgs that increase acute angle closure glaucoma?
Anti muscarinics TCI's
111
Treatment of herpes zoster ophtalmicus?
Oral aciclovir
112
Enlarging dark spot
Vitreous haemorrhage
113
Dense shadow
Retinal detachment

MRCP Opthalmology (1 decks)

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