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Year 4 - Special Senses > Ophthalmology - Progressive Visual Disturbances > Flashcards

Ophthalmology - Progressive Visual Disturbances Flashcards

1
Q

What are some causes of progressive visual loss?

A
  • cataracts
  • retinitis pigmentosa
  • age-related macular degeneration (ARMD)
  • diabetic retinopathy
  • primary open-angle glaucoma
  • ametropia
  • hypertensive retinopathy
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2
Q

Symptoms of chronic hypertensive retinopathy.

A

Hypertensive retinopathy due to chronic hypertension is usually asymptomatic and can only be diagnosed through clinical examination.

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3
Q

Symptoms of accelerated hypertensive retinopathy.

A

Acute rises in blood pressure causes symptoms:
- blurring of vision
- visual field defects
- headache
- facial plethora
- nausea and vomiting
- painless loss of vision due to vessel occlusion

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3
Q

Fundoscopic features of hypertensive retinopathy.

A
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4
Q

What grading system is used to classify hypertensive retinopathy?

A

Keith-Wagener-Barker classification

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5
Q

What grade of hypertensive retinopathy does malignant hypertension present with?

A

Grade 4 on Keith-Wagener-Barker classification:
- AV nicking
- flame haemorrhages
- cotton-wool spots
- hard exudates
- papilloedema

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6
Q

Imaging of hypertensive retinopathy.

A

Optical coherence tomography (OCT)

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7
Q

Management of hypertensive retinopathy.

A

Reduction of blood pressure.

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8
Q

Blood pressure targets for patients aged:

a) <80 years

b) ≥80 years

A

a) <135/85mmHg

b) <145/85mmHg

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9
Q

Management of accelerated hypertension.

A

Referral for same-day specialist assessment.

IV anti-hypertensives (e.g. labetalol, nicardipine) to reduce blood pressure over 24-48 hours*.

*reducing blood pressure too quickly may result in organ hypoperfusion.

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10
Q

Complications of hypertensive retinopathy.

A
  • retinal vessel occlusion
  • neovascularisation
  • vitreous haemorrhage
  • retinal detachment
  • progression of diabetic retinopathy
  • irreversible visual loss
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11
Q

Differential diagnosis to hypertensive retinopathy.

A

Diabetic retinopathy.

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12
Q

Ophthalmic complications of diabetes.

A
  • diabetic retinopathy
  • cataracts
  • cranial nerve palsy
  • retinal vessel occlusion
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13
Q

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

A
  • diabetic retinopathy
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14
Q

Risk factors for diabetic retinopathy.

A
  • length of exposure to hyperglycaemia
  • duration since diabetes diagnosis
  • hypertension
  • ethnicity
  • renal disease
  • pregnancy
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15
Q

Symptoms of diabetic retinopathy.

A

Usually asymptomatic, however:
- floaters
- blurred vision and distortion
- decreased visual acuity
- loss of vision
- blindness

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16
Q

Investigating diabetic retinopathy.

A

Bedside investigations:
- urinalysis (?glucosuria, proteinuria)
- visual acuity
- fundoscopy

Laboratory investigations:
- random plasma glucose
- HbA1c
- U&Es (end organ damage)
- LFTs (end organ damage)

Imaging:
- OCT

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17
Q

What are the fundoscopic classes of diabetic retinopathy?

A
  • non-proliferative
  • proliferative
  • diabetic macular oedema
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18
Q

Fundoscopic findings of non-proliferative diabetic retinopathy:

a) background retinopathy

b) pre-proliferative retinopathy

A

a) microaneurysms; dot and blot haemorrhages

b) hard exudates; cotton wool spots; venous veading; IRMAs

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19
Q

Fundoscopic findings of proliferative diabetic retinopathy.

A
  • neovascularisation
  • vitreous haemorrhage
  • retinal detachment
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20
Q

Symptoms of diabetic macular oedema (DMO).

A

As the macula is responsible for central vision, symptoms relate to this:
- blurred vision when reading
- difficulty recognising faces

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21
Q

What is the most common cause of visual loss in diabetic retinopathy?

A

Diabetic macular oedema (DMO).

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22
Q

Medical management of diabetic retinopathy.

A
  • glycaemic control
  • blood pressure control
  • diet, exercise and smoking cessation
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23
Q

HbA1c target for diabetics.

A

48-58mmol/mol

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24
Q

Primary intervention in management of proliferative diabetic retinopathy.

A

Photocoagulation - laser destruction of photoreceptors, decreasing retinal oxygen demand and delaying the progression of diabetic retinopathy.

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25
Q

What is

a) focal photocoagulation

b) pan-retinal photocoagulation

A

a) specific point of leakage is identified and targeted with a laser

b) periphery of the retina is targeted, aiming for a global reduction in oxygen demand

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26
Q

Complications of focal photocoagulation.

A
  • decreased quality of central vision
  • paracentral blind spot
  • worsening DMO
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27
Q

Complications of pan-retinal photocoagulation.

A
  • restricted peripheral vision
  • reduced quality of night vision
  • ocular pain
  • worsening DMO
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28
Q

What is the role of intravitreal anti-VEGF injections.

A

Minimises neovascularisation and thus are used in proliferative diabetic retinopathy.

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29
Q

Complications of intravetreal anti-VEGF injections.

A
  • cataract formation
  • increased intraocular pressure
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30
Q

Contraindications of intravetreal anti-VEGF injections.

A

Stroke or MI in the last 3 months.

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31
Q

Screening for diabetic retinopathy.

A

In the UK, the NHS provides an annual eye screening programme for any individual aged >12 with diabetes.

Aims to promptly identify and manage any changes associated with diabetic retinopathy.

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32
Q

Complications of diabetic retinopathy.

A
  • neovascular glaucoma
  • retinal detachment
  • vitreous haemorrhage
  • loss of vision
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33
Q

What is neovascular glaucoma?

A

Neovascularisation within the iris and its trabecular meshwork results in narrowing and closure of the drainage angle.

This results in an increased intraocular pressure.

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34
Q

Prognosis of untreated proliferative DR.

a) 2 years

b) 10 years

A

a) 50% lose vision in 2 years

b) 90% lose most vision in 10 years

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35
Q

What is the most common type of glaucoma?

A

Primary open-angle glaucoma (POAG).

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36
Q

Function of aqueous humour.

A

Supplies nutrients to the cornea and lens.

37
Q

Production and absorption of aqueous humour.

A

Produced by the ciliary body.

Travels through the posterior chamber through the pupil, to the anterior chamber.

Drains from the anterior chamber via the trabecular meshwork, into the canal of Schlemm.

38
Q

Pathophysiology of primary open-angle glaucoma.

A

Increased resistance to the outflow of aqueous humour through the trabecular network, into the canal of Schlemm.

This results in increased intraocular pressure, causing retinal ganglion cell death.

39
Q

Risk factors for POAG.

A
  • myopia
  • increased age
  • family history
  • cardiovascular disease
  • diabetes mellitus
40
Q

History of POAG.

A

Gradual loss of vision:
- peripheral vision
- superior visual field first
- central vision loss (end stage)

41
Q

Clinical findings of POAG.

A
  • increased IOP
  • visual field defects
  • fundoscopy (cupped optic discs)
42
Q

Investigations of POAG.

A
  • measuring intraocular pressure
  • slit lamp
  • visual field assessment
  • gonioscopy (open angle)
43
Q

What is the gold standard investigation to measure intraocular pressure?

A

Goldmann applanation tonometer

Non-contact tonometry involves shooting a small puff of air at the cornea and measuring its rebound; less accurate but useful for screening.

44
Q

Why must central corneal thickness be measured when suspecting glaucoma?

A

Intraocular pressure measurement can be affected by corneal thickness, and so allowances must be made.

45
Q

Management of POAG.

A
  • laser management
  • latanoprost eye drops
  • surgical trabeculectomy
46
Q

Complications of POAG.

A

Irreversible loss of vision.

47
Q

Driving counselling in POAG.

A

Legal responsibility to inform DVLA if:
- bilateral glaucoma (Group 1 drivers)
- unilateral glaucoma (Group 2 drivers)

48
Q

What is ametropia?

A

Visual disorders caused by abnormalities in the refractive power of the eye, leading to blurred vision.

49
Q

Main components of refraction for vision.

A
  • cornea (2/3)
  • lens
  • axial length
50
Q

Types of ametropia.

A
  • myopia
  • hypermetropia
  • astigmatism
  • presbyopia
51
Q

What is myopia?

A

State that occurs when the eye is too long, causing light to be focussed in front of the retina.

Myopia can also occur if the lens or cornea has a high focusing power, bringing the image forward in front of the retina.

52
Q

Risk factors for myopia.

A
  • genetic factors
  • excessive near reading
  • urbanisation
  • ambient lighting
  • nutrition
53
Q

Presentation of myopia.

A

Able to view objects held closely in front of eyes, owing to accommodation reflex.

Anything in the distance appears blurred.

54
Q

Management of myopia.

A

Concave (minus) lens

55
Q

What is hypermetropia?

A

State that occurs when the eye is too short, causing light to be focused behind the retina leading to blurred vision.

Also caused if the cornea or lens has a lower focusing power, meaning they form the image behind the retina.

56
Q

Presentation of hypermetropia.

A

Better visual acuity when viewing objects from afar, compared to near.

57
Q

Management of hypermetropia.

A

Convex (plus) lens

58
Q

What is astigmatism?

A

The cornea assumed a rugby shape or oval shape, as opposed to the normal spherical shape.

This causes the horizontal and vertical axis to differ in steepness, causing distortion of light.

59
Q

Management of astigmatism.

A

Cylindrical lens

60
Q

What is presbyopia?

A

Age-related weakness of the lens, meaning it is less able to perform accommodation.

Results in ability for near vision.

61
Q

What is age-related macular degeneration (AMD)?

A

Progressive loss of central vision associated with the formation of drusen, and changes in the retinal pigmentary epithelium.

Associated with ageing and most common cause of blindness in people over the age of 60.

62
Q

Risk factors for age-related macular degeneration.

A
  • age
  • ethnicity
  • family history
  • smoking
  • hypertension
  • diet
  • drugs (e.g. aspirin)
  • sunlight exposure
  • blue eyes
63
Q

What is the most common subtype of age-related macular degeneration (AMD)?

A

Dry AMD

64
Q

What is dry AMD?

A

Presence of asymptomatic drusen formation in Bruch’s membrane.

It is non-exudative and non-neovascular.

65
Q

What is wet AMD?

A

VEGF promotes angiogenesis and neovascularisation, resulting in formation of choroidal neovascular membranes (underneath the retina).

66
Q

Symptoms of AMD.

A

Progressive, central visual loss.

Worsened in low light settings.

67
Q

How to differentiate wet AMD and dry AMD in history.

A

Both present with progressive, central vision loss.

Wet AMD: rapid onset of symptoms; rapid visual deterioration.

Dry AMD: slow symptom onset; progressive visual deterioration.

68
Q

Common examination findings of AMD.

A
  • loss of central vision
  • Amsler grid (metamorphopsia)
  • fundoscopy
69
Q

Imaging of AMD.

A

Ocular coherence tomography (OCT).

70
Q

Management of dry AMD.

A
  • low vision refractory aids
  • vitamin supplements (AREDS2 formula) EARLY
71
Q

Management of wet AMD.

A

Urgent referral (<2 weeks).

Intravitreal anti-VEGF injections.

72
Q

Complications of intravitreal injections.

A
  • oedema of conjunctiva
  • scleral injection
  • grittiness/itching

RARE COMPLICATIONS (<1%):
- infection (endophthalmitis)
- retinal detachment
- cataract formation

73
Q

What is a cataract?

A

Opacification of the lens, particularly prevalent in elderly patients.

74
Q

Absence of the fundal reflex in the NIPE - diagnosis and management.

A

Congenital cataracts - urgent referral to ophthalmology.

Surgical management may be required in first 6 weeks of life, to prevent permanent visual loss due to brain neglecting the eye.

75
Q

Risk factors for cataracts.

A

Associated with age-related changes:
- diabetes
- steroid use
- UV exposure
- smoking
- ocular trauma
- genetic predisposition

76
Q

Symptoms of cataracts.

A
  • progressive blurring of vision
  • glare when looking at lights
  • colours appearing dull
77
Q

Signs of cataracts.

A
  • reduced fundal reflex
  • clouded lens
78
Q

Conservative mangement of cataracts.

A

Conservative management used unless symptoms affect lifestyle - focus on controlling risk factors:
- glycaemic control
- smoking cessation
- steroid use
- UV exposure

79
Q

Complications of cataracts.

A

Loss of vision

80
Q

Complications of surgical management of cataracts.

A
  • posterior capsule thickening
  • endophthalmitis
81
Q

What is retinitis pigmentosa?

A

Inherited retinal disorders causing retinal degeneration, leading to progressive vision loss.

82
Q

Genetics of retinitis pigmentosa.

A

Mutation of rhodopsin gene causes mutations in the genes encoding for proteins important for:
- photoreceptors
- retinal pigment epithelium

83
Q

Symptoms of retinitis pigmentosa.

A
  • reduced peripheral vision (tunnel vision)
  • night blindness
  • impaired dark adaptation
  • flashing lights
  • glare
  • reduced central vision

Rod photoreceptors are affected early, giving rise to above symptoms.

84
Q

Fundoscopy findings of retinitis pigmentosa.

A
  • bone-spicule retinal pigmentation
  • arteriolar attenuation
  • waxy optic disc pallor
85
Q

Bedside investigations for retinitis pigmentosa.

A
  • visual acuity assessment
  • confrontational visual field assessment
  • fundoscopy
86
Q

Specialist investigations for retinitis pigmentosa.

A
  • electroretinogram
  • perimetry
  • genetic testing
  • OCT (?cystoid macular oedema)
87
Q

Conservative management of retinitis pigmentosa.

A

Optimise vision:
- low vision aids (e.g. glasses, magnifiers)
- visual rehabilitation
- sunglasses (limit UV exposure)

88
Q

Complications of retinitis pigmentosa.

A
  • cataracts
  • cystoid macular oedema (CMO)
89
Q

Prognosis of retinitis pigmentosa.

A

No cure for retinitis pigmentosa.

Patients typically lose 50% of their remaining visual field every 5 years, however complete visual loss is rare.

Year 4 - Special Senses (17 decks)

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