Ophthalmology > Ophthalmology I > Flashcards

Ophthalmology I Flashcards

(123 cards)

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1
Q

Define cataracts

A

Any opacity or clouding of the lens
Progressive over years
Occurs bilaterally

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2
Q

List the risk factors for cataracts

A 
Sunlight
Age 
Smoking 
Alcohol 
Corticosteroids 
DM
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3
Q

Alternative causes of cataracts

A

Rubella
Wilson’s
Myotonic dystrophy

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4
Q

Presentation of cataracts

A

Increasing myopia
Blurred vision
Gradual vision loss
Monocular diplopia

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5
Q

Investigations for cataracts

A

Visual acuity
Dilated fundoscopy
Tonometery
Blood glucose to exclude DM

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6
Q

Management of catracts

A 
Cataract surgery 
Consider if several affecting the quality of life
Day case 
LA 
Phacoemulsification 
24hrs rehab 
insertion of intraocular lens
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7
Q

Complications of cataract surgery

A

Intraoperative

  • Ruptured lens capsule
  • Intraocular haemoorhage

Postoperative
- intraocular dislocation
- Capsule opacification
- Inflammation
- Intraocular infection (endophthalmitis)
Red painful eye with reduced vision, urgent intraocular abc are required

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8
Q

List the types of glaucoma

A

Open angle vs closed angle
Primary vs Secondary
Acute vs Chronic

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9
Q

Role of aqueous

A

Produced in the ciliary body
Circulated and nourishes the lens
Leaves the eye via trabecular meshwork in angle

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10
Q

What is intraocular pressure

A

Balance between the aqueous production and drainage
Impaired drainage raised intraocular pressure
Normal <21mmHg

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11
Q

Define chronic open angle glaucoma

A

Chronic progressive optic neuropathy

Changes in the optic nerve head and corresponding visual field loss

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12
Q

Presentation of chronic open angle glaucoma

A

Progressive visual field loss (tunnel vision): superior nasal first
Presentation is delaying until optic nerve damage is irreversible.

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13
Q

What is the triad seen in chronic open angle glaucoma

A
  1. Raised IOP (>21mmhg)
  2. Abnormal disc- cup ration asymmetry
  3. Visual field defect
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14
Q

Who is at high risk of developing the chronic open angle glaucoma

A 
>35yrs
Afro-Caribbean 
FH
Drugs (steroids) 
DM 
HTN
Migraines 
Myopia
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15
Q

Investigations for chronic open angle glaucoma

A

Tonometry
- IOP >21mmHG

Fundoscopy
Cupping of the optic disc

Visual field assessment: peripheral loss

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16
Q

Management of chronic open angle glaucoma

A

Life long f/up
Eye drops to decrease IOP to baseline pressure
1st line
- Timolol, bextaxolol
- decrease aqueous production
- caution in asthmatics and heart failure

2nd line

  • prostaglandin analogues
  • Latanoprost,

Others

  • Carbonic anhydrase inhibitors
  • Alpha antagonists (bromonidine)

Laser trabeculoplasty (only used if drugs fail)

Must review @ 6 weeks to assess response to treatment

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17
Q

List the causes of gradual vision loss

A

Common

  • Diabetic retinopathy
  • ARMD
  • Cataracts
  • Open-angle glaucoma

Rarer

  • Retinitis pigmentosa
  • Hypertension
  • Optic atrophy
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18
Q

Discuss visual acuity describing the role the macular plays

A

Macula lutea = part of the retina where the visual activity is highest
Temporal to the optic disc
Fovea: consist of cone photoreceptors
Visual acuity dependent on
1. Functional photoreceptors (rods/cones)
2. Healthy retinal pigment epithelium
3. Perfusion of the choroid (capillary layer)

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19
Q

List the risk factors for developing ARMD

A

Smoking
Increasing age
Genetic factors

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20
Q

Discuss the types of macular degeneration

A

First sign of aging: development of drusen

  1. Retinal atrophy: Dry AMD
    Slowly progression
  2. New vessel growth under the retina: Wet AMD
    Fast progressing
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21
Q

Describe the types of drussen

A
  1. Small white drussen
  2. Larger confluent soft drussen
  3. Crystalline hard drussen
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22
Q

Discuss the features seen in dry AMD

A

Atrophy of the RPE
Drussen: fluffy white spots around the macula
Central scotoma with preserved peripheral vision

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23
Q

Management and progression in dry AMD

A

Frequently deterioration
Require visual aids
Eligible for blind registration

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24
Q

Pathology of wet AMD

A

Aberrant vessels grow into retinas from choroid

Haemorrhage occurs

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25
Features seen on opthalmoscope in wet AMD
Choroidal neovascular membrane Leaking vessels below retina Exudates and haemorrhage and scarring
26
Presentation of wet AMD
Localised retinal detachment = distorted central vision Objects are distorted. Object appear smaller Development of central scotoma
27
Investigations for wet AMD
OCT: optical coherence tomography Provides high resolution images of the retina Amsler grid detects distortion
28
Management of wet AMD
Intravitreal injections anti-TNF-beta (pegantanib), (ranibizumab), Anti-VEGF (vascular endothethial growth factor A) Ohotodynamic laser post IV photosensitive vertoporfin if foveal
29
List the key features in sudden vision loss that would indicate the causes
Headache: GCA Eye movements hurt: optic neuritis Lights/flashing preceding visual loss: detached retina Like a curtain descending : TIA, GCA Poorly controlled DM: vitreous bleed from new vessels
30
Presentation of central retinal artery occulsion
``` Sudden total loss of vision Occurs in seconds Top half or bottom half lost: Branch retinal artery RAPD: Marcus Gunn Pupil Pale retina with cherry red macula ```
31
Causes of central retinal artery occlusion
1. Emboli carotid artery/ heart - Cartoid artery atheroma - Cholesterol - Cardiac valve 2. Giant Cell Arthritis 3. Thrombophilic conditions
32
Management of central retinal artery occulsion
``` If seen w/i 6hr - increase retinal blood flow by reduce IOP Ocular massage Surgical removal of aqueous Anti-hypertensives Very poor prognosis ```
33
Name the signs of ocular ischaemia syndrome
``` Retinal artery occlusion Blot haemorrhages Microaneurysms Dilated veins Rubeosis (abnormal vessel growth on iris) Reduced central artery perfusion pressure Late macular leakage Exacerbation of diabetic retinopathy ```
34
Name the investigation used for macroaneurysms
Fluorescein angiograpahy
35
Presentation of a branch retinal vein occlusion
Blurring of vision and visual field defect
36
Causes of branch retinal artery occlusion
``` Atherosclerosis HTN Diabetes Smoking Thrombophilias ```
37
What features are seen on an ophthalmoscope in incidence of branch retinal artery occlusion
``` Flame haemorrhages Leaking veins Intact arteries NB Must establish integrity of foveal arcadel ```
38
Management of branch retinal occlusions
1. Laser grid photocoagluation (guided by angiography) -indications Macula oedema Neovascularistation 2. Intravitreal triamcinolone (IVTA) (steriod suspension) - indications failure of photo coagulation contraindicated in glaucoma
39
Presentation of central retinal vein occulsion
Mild to severe loss of vision | +RADP
40
Features seen on ophthalmoscope central retinal vein occulsion
``` Widespread flame haemorrhages Swollen optic disc Dilated tortuous veins Extensive blot haemorrhages Worse centrally Macular oedema ```
41
List the causes of rubeosis
Diabetic retinopathy CRVO Ocular ischaemia Retinal detachment
42
Treatment of rubeosis
Panretinal photocoagulation | Vitrectomy
43
Pathology of Anterior ischaemic optic neuropathy
Optic nerve is damaged if ciliary arteries are blocked by inflammation or atheroma
44
Name the condtions (AION) is associated with
GCA
45
List the types of AION
Arteritic | Non arteritic
46
Presentation of AION and features of fundoscopy
Sudden and profound loss of vision RAPD Pale swollen optic disc
47
Treatment for AION
High dose steroids
48
Clinical features of optic neuritis
Unilateral loss of acuity Reduce colour discrimination Painful eye movements Optic disc may be swollen or blurred
49
Causes of optic neuritis
``` MS DM Drugs (ethambutol, chloamphenicol) Vitamin deficiency Zoster infection ```
50
Treatment of optic neuritis
High dose steroids
51
Pathology of retinal detachement
Potential space between the photoreceptors and the RPE fills with fluid Retina lifted or detached Leads to field defect
52
Presentation of retinal detachment
``` 4 F's Floaters Flashes Field loss Fall in acuity ``` PAINLESS
53
Features seen on fundoscopy in retinal detachment
Grey Opalescent retina Balloning forwards
54
Management of retinal detachement
Urgent surgery | Viterectomy + gas tamponade with laser coagulation to secure the retina
55
Name the causes of transient visual loss
``` Vascular TIA Migraine MS Subacute glaucoma Papilloedema ```
56
List the features seen in hypertensive retinopathy
1. Heightened reflex on artery (silver wiring) +/- Exudate 2. Microinfarct 3. Ateriovenous crossing change (vein disappears under the artery as the arterial wall thickens 4. Flame haemorrhages (superficial)
57
Name the classifcation criteria used in hypertensive retinopathy
Modified shceie
58
Complications of hypertensive retinopathy
``` Retinal vein occlusion Retinal artery occlusion AION Exacerbation of diabetic retinopathy Retinal macroaneurysms ```
59
List the features seen in retinopathy of accelerated hypertension
Extensive microvascular dilatation Choroidal (RPE) folds indicate swelling/detachement Lobular choroidal infarcts - Elschnig's spots - Siegrist streaks Extensive dilatation arteries and veins Retinal haemorrhages and microinfarcts (no nipping as acute)
60
List the causes of poor vision in accelerated HTN
``` Acute optic nerve damage Macular oedema Retinal artery closure Choroidal ischaemia Detachement Folds ```
61
Causes of accelerated HTN
``` Exacerbation of essential HTN Intrinsic renal disease Renal artery stenosis Phaeo Cushings Conn's ```
62
Pathology of diabetic retinoapthy
1. Microangiopathy in capillaries, precapillary arterioles and venues causes occlusion + leakage Results in ischaemia 2. New vessel formation in the retina + optic disc and iris = proliferative retinopathy 3. New vessels are fragile and can bleed (vitreous haemorrhage) Can result in retinal detachment Occlusions - cotton wool spots: ischaemic nerve fibres
63
Risk factors for diabetic retinopathy
``` Glycaemia control Systemic HTN Carotid stenosis Pregnacy Renal disease Lipids ```
64
Explain the progression of diabetic retinopathy
Background retinopathy - Dots - Blots - Hard exudates (yellow lipid patches) Pre-proliferative - Cotton wool spots (infarcts) - Venous bleeding - Dark haemorrhages - Intra retinal microvascular abnormalities Proliferative - New vessels - Pre-retinal or viterous haemorrhage - Retinal detachment Maculopathy - caused macula oedema - reduced acuity - hard exudates w/i one disc width of the macula
65
Features of maculopathy on fundoscopy
Retinal thickening Exudates approaching fovea Focal oedema (exudates and microaneurysms) Diffuse oedema
66
Screening for eye disease in diabetes
``` All diabetics should be screened annually Refer to opthalmologist those with - maculopathy - NPDR - PDR ```
67
Management of diabetic retinopathy
Optimise glycaemic control and BP NPDR (non severe) No macula oedema: observation Macula oedema: intravitreal anti VEGF + macular lens therapy NPDR (severe) No macula oedema: pan retinal photocoagulation Macula oedema: intra vitreal anti VEGF + macular laser therapy + pan retinal photocoagulation PDR (high risk) No macula oedema: urgent PRP Macula oedema: urgent PRP and intrvitreal anti VEGF + macula laser therapy Severe PDR Vitrectomy SE: Haemorrhage, cataract
68
Red eye red flags
``` Corneal inflammation: Keratitis Scleral inflammation: Scleritis Intraocular inflammation: Uveitis Intraocular infection: Endopthalmitis Raised IOP: Acute glaucoma ``` IMPAIRED VISION PAIN/PHOTOPHOBIA LACK OF OCULAR DISCHARGE
69
Define blepharitis
Chronic inflammation of the eyelid
70
Presentation of blepharitis
Gritty irritable eyes Wartery discharge Foreign body sensation eyelid
71
Management of blepharitis
Warm compress Lid massage Lid cleansing May require fusidic acid drops
72
Pathology of acute angle closure glaucoma
Blocked drainage of the aqueous from the anterior chamber via the canal of schlemm Pupil dilations (@ night) worsens the blocked IOP pressures increase 60mmHG
73
Risk factors for developing acute angle closure glaucoma
``` Hypermetropia Shallow ant chamber Female FH Increase age Drugs -anti cholinergics - sympathomimetics -TCAs - Anti-histamines ```
74
Symptoms of acute angle closure glaucoma
Prodrome: Rainbow haloes around lights at night time ``` Very red eye Corneal oedema Mid-dilated pupil Poor vision Severe pain Nausea and vomiting ```
75
Clinical signs of acute angle closure glaucoma
Cloudy cornea with circumcormeal injection Fixed dilated irregular pupil Increase IOP, eye feel hard
76
Investigations for acute angle closure glaucoma
Gonioscopy: trabecular meshwork not visible Slit lamp: shallow anteoir chamber, signs of glaucoma (large cup + nerve fibre loss) Static perimetery: visual field loss Tonometry: very high IOP (>40mmHg)
77
Management of acute angle closure glaucoma
1. Lower pressure Topical carbonic anhydrase inhibitors Topical beta blockers + oral acteazolamide (carbonic anydrase inhibitor) and intravenous mannitol ``` 2. Constrict the pupil Pilocarpine drops (topical cholinergic agonist) ``` 3. Prevent recurrence Laser +/- surgery Laser iridotomy: prevents a second attack by providing a bypass
78
What features make up the uvea
Iris Ciliary body Choroid
79
List the disease that are associated with acute anterior uveitis
1. Sero-negative arthropathies (HLA-B27) IBD Psoraitic arthritis Ankylosing spondylitis 2. Granulomatous disease Sarcoidosis Syphillis 3. Bechet's disease
80
Presentation of acute anterior uveitis
``` Acute painful red eye Unilateral Photophobia Blurred vision (acuity can range from normal to impaired) ```
81
Clinical signs of acute anterior uveitis
Intense redness of globe Irregular small pupil Normal to decreased visual acuity Hypopyom (pus and inflammation in the anterior chamber) Variable intraocular pressure (very low or very high)
82
Management of acute anterior uveitis
Dilate the eye: atropine and prednisolone eye drops Refer to ophthalmology Cyclophenolate drops: dilate the pupil and prevents adhesions between the iris and the lens (synechiae)
83
Presentation of episcleritis
``` Common Benign Mild irritation Localised redness No discharge No loss of vision ```
84
Treatment of episcleritis
Topical or systemic NSAIDs
85
Presentation of scleritis
Rare, serious and associated with systemic vasculitis Severe pain, worse on eye movement Conjunctivial oedema (chemosis) Generalised red eye
86
Management of scleritis
Refer to specialist Corticosteriods Immunosupressants
87
Presentation of conjunctivitis
``` Red eye Vision unaffected Purlent discharge Swollen Bilateral ``` If viral - watery - Sticky If bacterial - purulent
88
Causes of conjunctivitis
VIRAL Adenovirus presents with sudden onset red eye pre-auricular lymphadenopathy BACTERIAL Staphs Chlamydia Gonococcus
89
Management of conjunctivits
Bacterial Chloramphenicol drops 0.5% ointment Fusidic acid Good eye hygiene is essential
90
Management of opthalmia neonatorunm
Conjunctivits in the first 3 weeks of life Caused by Chlamydia (systemic infection) Gonorrhoea (loss of vision) Systemic erythromycin
91
Management of corneal abrasion disorders
Examine with a slit lamp using fluorescein dye (detect green) Chloramphenicol ointment for infection prophylaxis
92
Causes of keratitis
Viral - Herpes simplex - Characteristic shape (dendrite) stains green with fluorescein Bacterial
93
Presentation of keratitis
``` Pain Photophobia Conjunctival hyperaemia Reduced visual acuity White corneal opacity ```
94
Management of keratitis
``` Immediate referral specialist Take smears and cultures Abx drops, topical acyclovir if viral Mydriatics may ease photophobia Steriods may worsen symtpoms: professionals only ``` Comps: visual loss Scarring
95
Golden rules of red eye
Bilateral red eye is less serious than unilateral (conjunctivitis, blepharitis) Most benign causes resolve spontaneously Pain and loss of vision = serious - acute glaucoma - keratitis - scleritis - iritis Be cautious in prescribing topical steroids
96
Pathology of rentinitis pigmentosa
Hereditary progressive dystrophy of photoreceptors in the retina and the retina and the RPE
97
Presentation of retinitis pigmentosa
``` Night blindness Reduced visual fields Tunnel vision Central vision is spared Majority are registered blind by 30 ```
98
List the diseases which are associated with retinitis pigmentosa
Friedrich's ataxia | Usher's syndrome
99
Findings on fundoscopy in retinitis pigmentosa
Pale optic disc: disc atrophy | Peripheral retina pigementation: spares the macula
100
Management of retinitis pigmentosa
Refer tp ophthalmology + genetic counselling Screen complications (cataracts,glaucoma. macular oedema) Inform the DVLA Wear sunglasses Vitamin A/Beta carotene Acetazolamide
101
Name the layers of tear film
1. Watery layer from the lacrimal glands 2. Oily layer from the meibomian glands 3. Mucus layer from the conjunctiva
102
Causes of keratoconjunctivitis sicca
Aging Medications (diuretics, antidepressants, antihist, betablockers) Systemic illness (RA, SLE, Sjorgrens, hyposecretive) Blepharitis (decreased tear productions) Allergic conjunctivitis (decreased tear production) Increased evaporation
103
Presentation of dry eyes
Irritation Sight blurring Photophobia
104
Investigations for dry eyes
Slit lamp | Schirmer's test
105
Treatment of dry eyes
Artificial tears Drops (hypromellose, sodium chloride) Gels: cling to the surface of the eye (viscotears)
106
Management of allergic eye disorders
1. Remove allergen responsible where possible 2. General measure - Cold compress - Artificial tears - Oral antihistamines (loratadine 10mg/d PO) 3. Eye drops - Anti-histamines: azelastine - Mast cell stabilisers: cromoglycate - Steroids: dexamethasone - NSAIDs: Diclofenac
107
Pathophysiology of an orbital blowout fracture
Blunt injury to the eye | Sudden increase in orbital pressure with herniation of orbital contents into the maxillary sinus
108
Presentation of orbital blowout fracture
Ophthalmoplegia + Diplopia Tethering of inferior rectus + inferior oblique Loss of sensation to the lower lid skin Infraorbital nerve injury Ipsilateral epistaxis Damage to anterior ethmoidal artery Reduced acuity Irregular pupil that reacts slowly to light
109
Management of orbital blowout fracture
Refer to ophthalmologus | Refer to maxfax
110
Causes of floaters
``` Retinal detachement Viterous haemorrhage Diabetic retinopathy Old retinal branch occlusion Syneresis (degenerative opacities in the viterous) ```
111
Causes of flashes
``` Intraocular or intracereberal pathology Headache Nausea Vomiting Migraine Retinal detachement (in the presences of floaters) ```
112
Causes of halos
In the presences of eye pain | GLAUCOMA
113
Discuss the cause of myopia
Eyeball is too long | Correct with concave lens
114
Discuss the causes of hypermetropia
Eyeball is too short | Correct with convex lens
115
Name the types of squint
Convergent (common in children) | Divergent (intermittent)
116
Management of a non paralytic squint
3 O's Optical: correct refractive error Orthoptic: patching the good eye encourages use of the squinty eye Operations: resection and recessation of the recuss muscles
117
Causes of a third nerve palsy
``` Down and out DM Trauma Compression Multiple sclerosis Vascular Space occupying lesion ```
118
Causes of a fifth nerve palsy
``` Diplopia DM Trauma Compression Multiple sclerosis Vascular Space occupying lesion ```
119
Causes of a seventh nerve palsy
``` Medially deviated Cannot abduct DM Trauma Compression Multiple sclerosis Vascular Space occupying lesion ```
120
Pathology of orbital cellulitis
Infection spreads locally From paranasal sinuses, eyelid, external eye Caused by staphs, pneumococcus, GAS
121
Presentation of orbital cellulitis
``` Inflammation of the orbit Lid swelling Pain Decreased range of eye movement Exophthalmos Systemic signs (fever) Tenderness over the sinuses ```
122
Management of orbital cellulitis
IV abx: Cefuroxime (20mg/kg/8h IV)
123
List the stages in hypertensive retinopathy
Grade 1 - minimal arterial narrowing Grade 2 - arterial narrowing with focal irreg Grade 3 - grade 2 + haemorrhages +- exudates +- cotton wool Grade 4 - grade 3 + disc swelling (papilloedema)

Ophthalmology (1 decks)

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