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4. Senior Block- Special Senses > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

Which bones make up the orbit?

A 
Ethmoid
Zygomatic
Frontal 
Sphenoid
Lacrimal 
Palatine 
Maxilla
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2
Q

Give 3 functions of the eyelids

A

Protect eye from trauma
Protect eye from excessive light
Maintain lubrication of eyeball by distributing tears

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3
Q

Give the 6 orbital muscles

A 
Lateral rectus
Medial rectus
Superior rectus
Inferior rectus
Inferior oblique
Superior oblique
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4
Q

What nerve supplies the orbicularis oculi muscle and what does this muscle do?

A 
Facial nerve (CN VII)
Closes eyelids, helps to drain tears
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5
Q

What nerve supplies the levator palpebrae superioris and what does this muscle do?

A 
Oculomotor nerve (CNIII)
Opens the eyelid
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6
Q

Which ocular muscles does the oculomotor nerve supply?

A 
Medial rectus
Superior rectus
Inferior rectus
Inferior oblique
(Levator palpebrae superioris)
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7
Q

What nerve innervates the lacrimal gland and how does it act under autonomic innervation?

A

Lacrimal nerve, branch of opthalmic nerve, branch of the trigeminal nerve (CN V)
Parasympathetic –> increased secretion
Sympathetic –> decreased secretion

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8
Q

Describe the path of lacrimal fluid

A

Secreted from lacrimal gland via lacrimal ducts
Swept across eye via eyelids
Lacrimal canaliculi drain fluid into lacrimal sac
Enters nasolacrimal duct to enter the inferior meatus in the nose

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9
Q

What layer of the eye is known as the white of the eye?

A

Sclera

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10
Q

Give 3 roles of the cornea

A

Maintains transparency
Protects the eye
Refracts incoming light

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11
Q

What nerve innervates the cornea?

A

Long ciliary nerves from the opthalmic branch of the trigeminal nerve

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12
Q

What separates the anterior chamber from the posterior chamber of the eye?

A

The iris

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13
Q

Where does the aqueous humour drain?

A

The trabecular meshwork

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14
Q

What is mydriasis?

A

Dilation of the pupil via the dilator pupillae muscles. Sympathetic innervation in dull light

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15
Q

What is miosis?

A

Constriction of the pupil via the sphincter pupillae. Parasympathetic innervation in bright light

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16
Q

What is the role of the choroid?

A

Divides sclera and retina
Contains nerves and blood supply to the retina
Removes waste from outer retina
Reduces reflections by absorbing excess light

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17
Q

What are the 2 main layers of the retina?

A

Neural

Pigmented

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18
Q

What is the macula?

A

The center of the retina. Highly pigmented area

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19
Q

What is the fovea?

A

Area of the macula that has a high concentration of light detecting cells so is responsible for high acuity vision.

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20
Q

List the 6 extraocular muscles

A 
Lateral rectus 
Medial rectus 
Inferior rectus
Superior rectus
Superior oblique 
Inferior oblique
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21
Q

Where do the nasal fibres cross in the optic pathway?

A

Optic chiasm

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22
Q

What is the name of the nucleus in the brain that receives the optic tracts?

A

Lateral geniculate nucleus

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23
Q

What is a scotoma?

A

Blind spot

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24
Q

What condition may cause a central scotoma?

A

Macular degeneration

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25
Q

What factors may cause monocular visual loss?

A

Damage to the optic nerve

Trauma
Inflammation
Abscess

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26
Q

What condition may cause bitemporal hemianopia?

A

Pituitary adenoma

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27
Q

What conditions may cause homonymous hemianopia?

A 
Stroke 
Trauma 
Cerebral infection 
Brain tumours 
Abscess
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28
Q

Why do refractive errors occur?

A

Disorder of the size and shape of the eye

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29
Q

Describe the accommodation reflex

A

Far away object= lens is pulled to become thinner. Ciliary muscles relax and the suspensory muscles tighten

Close object= lens becomes thicker. Ciliary muscles contract so suspensory muscles loosen

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30
Q

What is myopia?

A

Short-sightedness
eye can focus on close by objects but not ones in the distance.

Due to a long axial length or the lens being too thick and curved.

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31
Q

What is hypermetropia?

A

Long-sightedness
Eye can focus on distant objects but not objects close by

Due to a short axial length or a loss of elasticity in the lens. Associated with advancing age (presbyopia)

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32
Q

What is astigmatism?

A

The cornea does not have the same degree of curvature along its whole surface so images are focussed at different points on the retina.

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33
Q

What is a squint/strabismus?

A

Eyes are misaligned

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34
Q 
With regard to a squint, what do these terms mean:
Eso- 
Exo-  
Hyper-  
Hypo-
A 
Eso = turning in 
Exo = turning out 
Hyper = looking up 
Hypo = looking down
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35
Q

What is a concomitant squint?

A

Angle of the squint is the same in all directions of gaze

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36
Q

What is an non concomitant squint?

A

Angle of the squint varies with gaze

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37
Q

What is a convergent squint?

A

Esotropia

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38
Q

What is a divergent squint?

A

Exotropia

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39
Q

What is the most common type of squint in young children?

A

Esotropia- one eye turned in

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40
Q

What 2 tests can be done to investigate a squint?

A

Corneal reflection- reflection of bright light will not be symmetrical

Cover test- movement of the uncovered eye to fixate as the other eye is covered will suggest a manifest squint

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41
Q

Describe the results of a cover test in a left convergent (esotropic) squint

A

Left eye covered, right eye focuses

Right eye covered, left eye moves out to take up fixation

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42
Q

Describe the results of a cover test in a left divergent (exotropic) squint

A

Left eye covered, right eye focuses

Right eye covered, left eye moves in to take up fixation

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43
Q

Give 3 reasons to treat a squint

A

Leads to amblyopia (lazy eye)
Reduced coordination
Psychosocial effects
May have sinister underlying cause

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44
Q

Give the 3Os for treating a squint

A

Optical –> assess for refractive errors and prescribe glasses

Orthoptic –> pathing the good eye forces the squint to focus

Operation –> can have resection and recession of the rectus muscles. Helps alignment and gives good cosmetic results

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45
Q

Describe the ocular presentation of a 3rd nerve palsy

A

Ptosis
Proptosis
Fixed pupil dilation

“Down and out” pupil

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46
Q

Give 3 causes of a 3rd nerve palsy

A

Cavernous sinus lesion
Diabetes
Cranial tumour
PCA aneurysm

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47
Q

Describe the ocular presentation of a 4th nerve palsy

A

Diplopia
Head tilt
Cannot look down and in, SO paralysed

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48
Q

Give 3 causes of a 4th nerve palsy

A

Trauma
Diabetes
Brain tumour
Idiopathic

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49
Q

Describe the ocular presentation of a 6th nerve palsy

A

Horizontal diplopia

Eye cannot move laterally as LR paralysed

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50
Q

Describe the pupillary light reflex

A

As light is shone in one eye, the impulses travel down the optic nerve and optic radiations to the visual cortex in the occipital lobe and synapse on BOTH left and right Edinger-Westphal nuclei.

The efferent pathway made up of cranial nerve III, synapses at the ciliary ganglions and then acts on BOTH eyes to either constrict the pupils.

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51
Q

What is the meaning of the consensual light reflex?

A

Both pupils constrict when light is only exposed to one eye

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52
Q

What happens to the pupil in bright light?

A

Constricts- via circular muscles contracting

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53
Q

What happens to the pupil in dim light?

A

Dilates- via radial muscles contracting

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54
Q

Give 3 causes of an afferent defect

A

Optic neuritis
Optic atrophy
Retinal disease

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55
Q

Explain the pathophysiology of an afferent defect

A

Eg. Light shone in right eye. Right optic nerve damaged so no afferent conduction (via optic nerve) to the cortex. Therefore, no consensual pupil constriction in the left eye.

Light shone in the left eye. Signal sent to the optic nuclei and consensual reflex present so right will also constrict as the efferent pathway is still intact.

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56
Q

What test can be done to prove a Relevant Afferent Pupillary Defect (RAPD)?

A

Swinging flashlight test

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57
Q

Explain the swinging flashlight test

A

Left eye damaged

Light in Left eye= eye constricts poorly to light and consensual response in the right hand side (half constricts)

Light in right eye= eye constricts fully to light and consensual response in the left means it also constricts fully

Light in left eye again = left eye dilates instead of constricts as perception of the light is poor

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58
Q

What is the cause of an efferent pupillary defect?

A

3rd Nerve Palsy

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59
Q

Give 3 causes of a fixed dilated pupil

A

Mydriatics
Trauma
Acute glaucoma
Coning

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60
Q

What is a Tonic (Adie) pupil?

A

Lack of parasympathetic innervation results in poor constriction to light. Presents with sudden blurring of vision, often in young women

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61
Q

How does Horner’s Syndrome present ocularly?

A

Miotic pupil

No dilation in the dark

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62
Q

Give 2 causes of Horner’s Syndrome

A

Pancoast tumour
MS
Aortic aneurysm

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63
Q

What is an Argyll Robertson pupil?

A

Bilateral miosis
Poor pupillary dilation
Pupil irregularity
Accommodates but does not react

Associated with diabetes and syphilis

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64
Q

Give 4 predisposing factors for cataract formation

A 
Increasing age 
Diabetes 
Smoking 
Trauma to lens 
High myopia
Excess alcohol 
FHx of cataracts 
Long term steroid use 
Genetics
HIV Positive
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65
Q

What is a cataract?

A

A cataract is the loss of transparency/opacity of the lens. Can result from disruption to the lens fibres configuration, capsule or epithelium

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66
Q

Describe the 3 types of cataracts

A

Subcapsular= located directly under the lens capsule. Has a granular or plaque appearance. Quick progression and cause glare from bright light.

Nuclear= Involves lens nucleus. Patient becomes myopic due to increase in refractive index. Colours appear more yellow/brown

Cortical= in the cortex of the lens. Radial wedge shaped opacities which cause astigmatic changes

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67
Q

Give 4 clinical features of cataracts

A

Blurred vision
Loss of stereopsis- judging distance
Gradual painless loss of vision
Difficulty driving at night due to glare of lights
Colour vision dampened- see more yellows/browns

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68
Q

Give 3 indications for cataract surgery

A

Troubling symptoms
Lifestyle is restricted
Can no longer drive

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69
Q

What is the name of cataract surgery?

A

Phacoemulsification +/- lens transplant

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70
Q

Describe the process of cataract surgery

A

Day case procedure under LA. Small incision made and lens removed by phacoemulsion. (lens broken down using ultrasound pulsed and then sucked out via a cannula).

A new lens is folded and then inserted into the eye

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71
Q

What investigation is done prior to cataract surgery?

A

Ocular biometry- measures curvature of cornea and length of eye to predict best lens implant

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72
Q

What is the post-op care for post cataract surgery?

A

Can return home straight away afterwards
Need antibiotic and anti-inflammatory drops for 3-6 weeks
Need to change glasses prescription

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73
Q

Give 4 potential complications of cataract surgery

A 
Posterior capsule thickening
Astigmatism 
Eye irritation 
Anterior uveitis
Vitreous haemorrhage
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74
Q

Give 4 predisposing factors for open angle glaucoma

A 
Fhx of glaucoma
African-American/Latino 
Diabetic
CV disease
Increasing age 
Hypertension
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75
Q

What is the pathophysiology of chronic glaucoma?

A

Obstruction in drainage of the aqueous humour via the trabecular meshwork leads to increase in intraocular pressure. There is a wide gap between the iris and the cornea.

The increased intraocular pressure (>21 mmHG) causes optic neuropathy with death of retinal ganglion cells and their optic nerve axons.

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76
Q

Give 3 clinical features of open angle glaucoma

A

Asymptomatic for many years- picked up incidentally

Symptoms bilateral:
Blurred vision
Visual field loss - irreversible
Difficulty crossing busy roads

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77
Q

Who is invited to open angle glaucoma screening?

A 
>35 years old
Afro-Caribbean 
Myopia 
Diabetic eye disease
Thyroid eye disease
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78
Q

Why is screening important in chronic glaucoma?

A

Asymptomatic disease until visual field loss but by this point the symptoms are irreversible

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79
Q

Give 4 investigations that can be done to assess open angle glaucoma and what they look for

A
  • Tonometry= measures the intraocular pressure
  • Perimetry= measures visual fields
  • Gonioscopy= visualises anterior chamber drainage to see if angle is open or closed
  • Fundoscopy with slit lamp= assesses if there is optic disc cupping- optic disc atrophy + wider and deeper so the vessels look like they have breaks.

(- OCT= looks for damage to the retina)

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80
Q

How is open angle glaucoma managed medically?

A
  • Prostaglandin analogues= increase uveoscleral outflow
  • Beta blockers (Timolol)= decrease production of aqueous
  • Alpha-adrenergic agonists= decrease production of aqueous
  • Carbonic anhydrase inhibitors= decrease production of aqueous
  • Miotics (Pilocarpine)= decrease resistance to aqueous outflow
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81
Q

What is trabeculoplasty?

A

Laser therapy to increase aqueous outflow to reduce intraocular pressure.

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82
Q

What surgery can be done to treat open angle glaucoma?

A

Trabeculectomy- puts pressure valve in the border of the sclera and the cornea

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83
Q

What is the function of rod cells?

A

Sense contrast and motion. Assist in seeing in darker environments

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84
Q

What is the function of cone cells?

A

Sense fine detail and colour vision

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85
Q

Describe the blood supply to the retina

A

Inner 2/3rds= central retinal artery

Outer 1/3rd= choroidal blood supply

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86
Q

What are the 3 mechanisms of retinal detachment?

A

Rhegmatogenous= retinal tears result in retinal fluid passing from the vitreous space to the subretinal space which peals the retina away

Exudative= subretinal fluid accumulation without a tear. Occurs due to diabetes, hypertension, vasculitis, macular degeneration or tumours

Tractional= formation of vitreoretinal bands which pull on the retina as the eye moves.

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87
Q

What is retinal detachment?

A

Detachment of the neurosensory retina from the retinal pigment epithelium. Loss of retinal function due to disturbed metabolic processes. If detached for >12 hours there is retinal ischaemia and degeneration

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88
Q

Give 3 predisposing factors for rhegmatogenous retinal detachment

A 
Severe myopia 
Previous intraocular surgery 
Posterior vitreous detachment 
Trauma
Retinal detachment of contralateral eye
Family history
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89
Q

Give 3 predisposing factors for exudative retinal detachment

A 
Pre-eclampsia 
Diabetes 
Hypertension 
Penetrating eye trauma 
Retinoblastoma
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90
Q

Give 3 predisposing factors for tractional retinal detachment

A

Proliferative diabetic retinopathy
Retinopathy of prematurity
Sickle cell retinopathy

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91
Q

Give 4 clinical features of retinal detachment

A 
4 Fs: 
Floaters
Flash of light (photopsia) 
Field loss (scotoma) 
Fall in acuity

Sudden painless loss of vision
RAPD

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92
Q

What is seen on fundoscopy in retinal detachment?

A

Grey, opalescent retina
Balloons forward
May be able to see retinal tear- retina floats freely in vitreous

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93
Q

How is a retinal detachment managed conservatively?

A

Rest

Posture- if superior detachment, lie flat. If inferior detachment, lie 30 degrees head up

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94
Q

How is a minor retinal detachment managed?

A

Laser photocoagulation

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95
Q

How is a major retinal detachment managed?

A

Prompt surgery:
Vitrectomy
External/internal tamponade= close tear

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96
Q

What is retinitis pigmentosa?

A

Progressive hereditary dystrophy of the retina which starts between ages 5-30 years

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97
Q

Give 4 clinical features of retinitis pigmentosa?

A 
Night blindness
Narrowing field of vision 
Glare sensitivity
Defects in colour and contrast perception
Late stage= blindness
98
Q

How is retinitis pigmentosa investigated?

A

Fundoscopy= pattern of dark spots
Perimetry= test field of vision
Electroretinography

99
Q

How is retinitis pigmentosa managed?

A

No known cure
Inform DVLA
Psychological support

100
Q

What is posterior vitreous detachment?

A

Detachment of the posterior vitreous cortex from the internal limiting membrane of the retina.

Due to age related degeneration of the vitreous body, myopia or eye injury

101
Q

Give 2 symptoms of posterior vitreous detachment

A

Asymptomatic
Floaters
Photopsia with eye movements

102
Q

What is seen on slit lamp examination in posterior vitreous detachment?

A

Irregular ring= visible posterior vitreous

103
Q

How is posterior vitreous detachment managed?

A

No treatment if no symptoms

If symptoms present treat the cause eg. retinal detachment, retinal hole

104
Q

What is a vitreous haemorrhage?

A

Extravasation of blood in the vitreous body

105
Q

Give 3 potential mechanisms for vitreous haemorrhage

A
  • Rupture of neovascular vessels in ischaemic changes of the retina eg. proliferative diabetic retinopathy, retinal vein occlusion
  • Rupture of physiological vessels eg. symptomatic posterior vitreous haemorrhage, retinal tear
  • Haemorrhage from adjacent site eg. tumour macroaneurysm
106
Q

Give 3 clinical features of vitreous haemorrhage

A 
Floaters
Visual loss
Unilateral, painless
Worse after sleep
No red reflex in severe cases
107
Q

What can be seen on slit lamp examination of vitreous haemorrhage?

A

Blood between vitreous base and limiting membrane

108
Q

How is vitreous haemorrhage managed?

A

Watch and wait
Treat underlying cause
+/- Vitrectomy

109
Q

Give 3 predisposing factors for retinal vein occlusion

A 
>80 years old
Atherosclerosis
Hypertension 
Diabetes 
Glaucoma 
Vasculitis
110
Q

How does ischaemic retinal vein occlusion present?

A

Sudden, severe loss of vision in affected eye

RAPD

111
Q

How does non-ischaemic retinal vein occlusion present?

A

Subacute, mild to moderate loss of vision, no RAPD

112
Q

How does retinal vein occlusion look on fundoscopy?

A

Dot and blot and/or flame haemorrhages in all 4 quadrants

Ischaemic= cotton wool spots, macular oedema, papilloedema

113
Q

How is retinal vein occlusion managed?

A

Laser therapy
Intravitreal injection of VEGF-inhibitors
Panretinal photocoagulation

114
Q

How is retinal vein occlusion investigated?

A

Fluorescein angiography- can see if it is ischaemic or not

115
Q

Give 4 predisposing factors for retinal artery occlusion

A 
Carotid artery atherosclerosis 
Atrial fibrillation 
Vasculitis
>60 years old
Male
116
Q

Give 3 features of retinal artery occlusion

A

Sudden painless loss of vision in one eye
Descending curtain visual loss
RAPD

117
Q

How does retinal artery occlusion present on ophthalmoscopy?

A

Grey discolouration of the entire retina

Cherry red spot at the fovea centralis

118
Q

How is retinal artery occlusion investigated (non-eyes)?

A

Carotid doppler
Echocardiogram
Rule out temporal arteritis- ESR, temporal artery biopsy

119
Q

How is retinal artery occlusion managed?

A

Medical emergency

Eyeball massage
Carbogen therapy
Decrease intraocular pressure
Vasodilators

120
Q

Describe the 2 mechanisms of developing retinoblastoma

A
  • Heritable= autosomal dominant mutation on 1 of the retinoblastoma (Rb) alleles plus a spontaneous mutation of the other Rb allele resulting in a non-functioning Rb gene –> Retinoblastoma (bilaterally)
  • Sporadic= two spontaneous mutations in the same cell affecting both Rb alleles. Tends to be unilateral
121
Q

At what age does retinoblastoma present?

A

<3 years old- most common childhood intraocular malignancy

122
Q

Give 4 clinical features of retinoblastoma

A 
Leukocoria (white pupillary reflex) 
Strabismus (squint) 
Painful red eye 
Loss of vision 
Advanced= retinal detachment
123
Q

What is seen on fundoscopy in retinoblastoma?

A

Greyish-white vascularised retinal tumour

124
Q

How is retinoblastoma investigated?

A

Ocular US
Contrast MRI of head
Genetic testing for Rb1 gene- can screen siblings

125
Q

How is retinoblastoma managed if the eye is salvageable?

A

Cryotherapy
Photocoagulation
Brachytherapy
Chemotherapy

126
Q

How is retinoblastoma managed if the eye is not salvageable?

A

Enucleation= removal of eye

Adjuvant high dose chemotherapy

127
Q

Give 3 signs of poor prognosis in retinoblastoma

A

Late diagnosis
Tumour grown into choroidal layer of optic nerve
Bilateral involvement

128
Q

What is a macular hole?

A

Vitreous loses some water content which causes it to shrink causing traction on the retinal tissue. This causes a small tear in the macular region of the retina.

No associated with retinal detachment

129
Q

How does a macular hole present?

A

Distorted vision and blurring

Visual loss

130
Q

What can be seen on fundoscopy and slit lamp examination of a macular hole?

A

Fundoscopy= small punched out area on the macula with yellow-white deposits

Slit lamp= round excavation with well defined edges and grey halo

131
Q

How is a macular hole managed?

A

Watch and wait (early cases)
Vitrectomy
Tamponade= air bubble put in vitreous to put macular back in position

132
Q

Give 5 risk factors for Age-related macular degeneration (ARMD)

A 
>55 years old
Female 
White 
CV disease
Hx of cataract surgery 
Increasing age 
FHx and genetics 
Smoking 
Obesity
133
Q

What is the pathophysiology of Wet Age-related macular degeneration (ARMD)?

A

10% of Age-related macular degeneration (ARMD)

Pathological choroidal neovascular membranes develop under the retina. Fluid and blood leaks out of the vessels to result in sudden localised elevation of the macula and detachment of the retinal pigment epithelium

134
Q

Describe the onset of Wet Age-related macular degeneration (ARMD)

A

Acute or insidious onset over weeks to months

Presents unilaterally first

135
Q

What is seen on fundoscopy in Wet Age-related macular degeneration (ARMD)?

A

Fluid exudation
Detachment of the retina
Fibrous disciform scars
Grey retinal discolouration

136
Q

What is the pathophysiology of Dry Age-related macular degeneration (ARMD)?

A

90% of Age-related macular degeneration (ARMD)

Deposition of yellow-white material in and under the retinal pigment epithelium (drusen). Results in slow progressive atrophy of the retinal pigment epithelium

137
Q

Describe the onset of Dry Age-related macular degeneration (ARMD)

A

Slow progressive visual impairment over decades. Can be unilateral or bilateral

138
Q

What is seen on fundoscopy in Dry Age-related macular degeneration (ARMD)?

A

Drusen
Mottling
Retinal pigment epithelium atrophy

139
Q

Give 4 clinical features of Age-related macular degeneration (ARMD)

A 
Contrast perception difficulty 
Hard to read and make out faces
Poor night vision 
Visual fluctuations 
Scotoma 
Metamorphopsia= distortion of visual images
140
Q

How is Age-related macular degeneration (ARMD) investigated and what extra tests can be done for Wet ARMD?

A

Fundoscopy
Amsler grid

Wet= OCT of macula, colour fundus photography, fluorescence angiography

141
Q

How is Dry Age-related macular degeneration (ARMD) managed?

A 
Supportive treatment
Decrease risk factors- stop smoking, lose weight
Antioxidants 
Increase vegetables in the diet 
Patient education
142
Q

How is Wet Age-related macular degeneration (ARMD) managed?

A

4-6 weekly reviews
Stop smoking
Increase green leafy vegetable intake

1st line= VEGF inhibitor injection into vitreous body
2nd line= Laser coagulation, photodynamic therapy

143
Q

What is papilloedema?

A

Optic disc swelling caused by raised intracranial pressure. Almost always bilateral

144
Q

Give 3 causes of papilloedema

A

Space occupying lesion
Malignant hypertension
Hydrocephalus
Hypercapnia

145
Q

Give 4 signs on fundoscopy of papilloedema

A 
Venous engorgement 
Loss of venous pulsation 
Blurring optic disc margin 
Elevation of optic disc 
Loss of optic cup
146
Q

What symptoms may be present alongside papilloedema?

A 
Headaches 
Nausea
Vomiting 
Diplopia 
Pulse like ringing in the ears
147
Q

Give 3 risk factors for optic atrophy

A

Glaucoma
Ischaemia
Compression of optic nerve
Hydrocephalus

148
Q

What is optic atrophy?

A

Death of the retinal ganglion cell axons that comprise the optic nerve. Occurs secondary to optic nerve damage.

Loss of axons + shinkage of myelin leading to gliosis and optic cup widening

149
Q

Give 2 clinical features of optic atrophy

A

Visual loss
Scotoma
Colour blindness

150
Q

What is seen on fundoscopy in optic atrophy?

A

Pale optic disc

Sharp edges

151
Q

What is an optic nerve head drusen and what does it look like on fundoscopy?

A

Globular calcified hyaline bodies located in the optic nerve head. Often an incidental finding

Fundoscopy= blurred optic disc, irregular margins, pseudopapilledema, yellow-white nodules

152
Q

What is optic neuritis?

A

Inflammation of the optic nerve commonly due to MS

153
Q

Give 4 clinical features of optic neuritis

A

Unilateral decrease in visual acuity over days
Poor discrimination of colours- red desaturation
Pain on eye movements
RAPD
Central scotoma

154
Q

How is optic neuritis managed?

A

High dose steroids

Will recover in 6 weeks

155
Q

What is the pathophysiology of giant cell arteritis?

A

Cell-mediated immune response to endothelial injury. Results in inflammation and local vascular damage.

156
Q

Give 3 risk factors for giant cell arteritis

A 
Polymyalgia rheumatica 
Women
>50 years old 
Genetic predisposition 
White
157
Q

Give 5 clinical features of giant cell arteritis

A 
Fever 
Weight loss
New onset onset 
Loss of vision 
Night sweats
Fatigue/malaise
Jaw claudication 
Diplopia
158
Q

How is giant cell arteritis diagnosed?

A

Need 3/5 of:

  • > 50 years
  • Headaches
  • Temporal artery abnormality
  • Raised ESR (>50mm/h)
  • Histopathological abnormalities (from temporal artery biopsy)
159
Q

How is giant cell arteritis managed?

A

High dose IV glucocorticoids –> prevents vision loss
Low dose aspirin

Low dose oral glucocorticoids for 1-2 years

160
Q

Give 3 complications of giant cell arteritis

A

Permanent vision loss
Cerebral ischaemia
Aortic aneurysm

161
Q

Give 3 causes of orbital cellulitis

A

Tooth infection
Otitis media
Orbital trauma
Ophthalmic surgery

162
Q

What is orbital cellulitis?

A

Infection of orbital contents such as the fat and extraocular muscles. Globe is not affected. It is a complication of URTIs especially bacterial rhinosinusitis

163
Q

Give 4 clinical features of orbital cellulitis

A 
Proptosis
Ophthalmoplegia
Fever 
Malaise
Reduced vision 
Diplopia 
RAPD
Ocular pain 
Eyelid swelling
164
Q

How is orbital cellulitis managed?

A

Empirical IV antibiotics

Vancomycin + Ceftriaxone/Ciprofloxacin for 1-2 weeks

165
Q

Give 3 predisposing factors of acute angle glaucoma

A 
Female
Advanced age 
Mydriasis
Asian 
Eye injury
166
Q

What is the pathophysiology of acute angle glaucoma and what is the difference between primary and secondary

A

Blocked trabecular network causes raised intraocular pressure

Primary= due to anatomical features

Secondary= due to scaring, lens luxation etc

167
Q

Give 5 clinical features of acute glaucoma

A 
Unilateral, inflammed, reddened and severely painful eye 
Frontal headache 
Nausea and vomiting 
Blurred vision + halo around light 
Cloudy cornea 
Unresponsive pupil- mid-dilated

Sudden onset- rapid, permanent vision loss

168
Q

How is acute angle glaucoma investigated?

A

Hard globe on palpation
Slit lamp
Gonioscopy (Gold standard)
Tonometry

169
Q

How is acute angle glaucoma managed?

A

Eye drops- Timolol (beta-blockers), Apraclonidine
Carbonic anhydrase inhibitor oral/IV- Acetazolamide
Topical cholinergics- Pilocarpine
Analgesia
Antiemetics
Surgery= Iridotomy

170
Q

How is chemical conjunctivitis managed?

A

Irrigate with water until the pH returns to normal

171
Q

Give 3 predisposing factors for retrobulbar haemorrhage

A

Vomiting after eye surgery
Hypertension
Orbital trauma
Anticoagulation

172
Q

What is the pathophysiology of retrobulbar haemorrhage

A

Rare, rapidly progressing sight-threatening emergency due to accumulation of blood in the retrobulbar space.

Can lead to increased IOP, stretching of the optic nerve and blockage of vascular structures supplying the eye.

173
Q

What are the clinical features of retrobulbar haemorrhage

A 
Eye pain 
Periorbital bruising 
Eyelid haematoma 
Proptosis 
Visual loss 
Nausea and vomiting
174
Q

How is retrobulbar haemorrhage managed?

A

Rapid intervention to prevent visual loss

Decompress orbit surgically

175
Q

What is Keratoconjunctivitis sicca?

A

Unable to produce enough tears resulting in dry eyes

176
Q

What conditions is Keratoconjunctivitis sicca associated with?

A 
Diabetes
Sjogren's
Thyroid disorders
RA
Lupus
177
Q

Give 3 predisposing factors for Keratoconjunctivitis sicca

A

> 50 years
Female
Low vitamin A
Contact lens use

178
Q

Give 4 clinical features of Keratoconjunctivitis sicca

A 
Stinging 
Scratching 
Red eye 
Photophobia 
Watery eyes 
Blurred vision 
FB sensation
179
Q

How is Keratoconjunctivitis sicca prevented?

A 
Sunglasses
Take eye breaks from screens 
Dehumidifier 
Stop smoking 
Artificial tears
180
Q

What is blepharitis?

A

Inflammation of the rims of the eyelids associated with seborrhoeic dermatitis, rosacea and acne

181
Q

Give 3 symptoms of blepharitis

A

Burning
Sore eyes
Itching
Lid cysts

182
Q

How is blepharitis managed?

A

Eye hygiene
Lid cleaning
Topical antibiotics
No cure- will have repeated episodes

183
Q

What is herpes zoster ophthalmicus (HZO)?

A

HSV infection of ophthalmic branch of cranial nerve V

184
Q

Give 4 symptoms of herpes zoster ophthalmicus (HZO)§

A 
Pain 
Altered sensation on forehead unilaterally 
Malaise 
Headaches 
Fever

Eyes= vesicles on lid margins, episcleritis, keratitis, anterior uveitis, secondary glaucoma

185
Q

How is herpes zoster ophthalmicus (HZO) managed?

A 
Rest and fluids 
Avoid contact with elderly or pregnant 
Pain relief 
Topical lubricants 
Systemic antivirals
186
Q

What is a hyphema?

A

A hyphema is an anterior chamber haemorrhage. The blood pools and can block the iris resulting in vision being blocked. It is painful and can cause permanent vision problems

187
Q

Give 3 causes of hyphema

A

Trauma
Sickle cell
Haemophilia

188
Q

Give 3 clinical features of hyphema

A

Visible blood in the front of the eye
Photophobia
Pain
Cloudy vision

189
Q

How is a hyphema managed?

A

Patch over the eye
Bed rest
Limit eye movements
Daily eye pressure checks

190
Q

What is a corneal abrasion?

A

Scratch of corneal epithelium

191
Q

Give 4 causes of a corneal abrasion

A 
Foreign body 
Entropion 
Prolonged contact lens use 
UV light 
Thermal burn 
Dry eyes 
Trauma
192
Q

How is a corneal abrasion diagnosed?

A

Fluorescein staining

193
Q

How is a corneal abrasion managed?

A

Removal of foreign bodies
Analgesia
Infection prophylaxis
Eye patching

194
Q

What is the prognosis of corneal abrasion

A

Usually heals within 48 hours with no follow up needed.

195
Q

What is a corneal erosion?

A

Detachment of the corneal epithelium from the tissue layers below including the basement membrane and Bowman’s membrane

196
Q

Give 3 causes of corneal erosion

A 
Corneal dystrophy 
Corneal ulcer
Contact lens use 
Diabetes
Dry eye
197
Q

What is keratitis?

A

Inflammation of the cornea which can lead to irreversible vision loss

198
Q

Give 3 risk factors for bacterial keratitis

A

Contact lens use
Recent eye surgery
Immunodeficiency

199
Q

Give 2 potential bacterial causes of bacterial keratitis

A

Staph aureus
Strep pneumoniae
P. aeruginosa
Syphilis

200
Q

What are the clinical features of bacterial keratitis

A 
Eye pain 
FB sensation 
Purulent discharge 
Photophobia
Tearing 
Blurry vision 
Red eye
201
Q

How is bacterial keratitis diagnosed?

A

Slit lamp and fluorescein staining +/- cultures

202
Q

How is bacterial keratitis managed?

A

Topical broad spectrum antibiotics

Corticosteroids

203
Q

What is herpes simplex keratitis?

A

Inflammation of the cornea due to reactivated HSV1 in the trigeminal ganglion

204
Q

How is herpes simplex keratitis managed?

A

Topical ganciclovir
Oral aciclovir
Corneal transplant

205
Q

What is herpes zoster keratitis?

A

Inflammation of the cornea due to reactivated HZV when ophthalmic nerve involved (shingles)

206
Q

How is herpes zoster keratitis managed?

A

Oral aciclovir

207
Q

What is posterior uveitis?

A

Inflammation of vitreous body, choroid and retina

208
Q

Give 4 potential causes of posterior uveitis

A 
CMV
EBV
Syphilis 
TB 
Toxoplasmosis 
Rubella 
HSV
VZV
Bechets 
SLE 
IBD
Wegener's
209
Q

How does posterior uveitis present?

A

Floaters
Scotoma
Blurred vision

210
Q

What is seen on ophthalmoscopy in posterior uveitis?

A

Leukocytes in vitreous humour

211
Q

What is anterior uveitis?

A

Inflammation of iris and ciliary body

212
Q

Give 3 causes of anterior uveitis

A 
Idiopathic 
RA
Sarcoidosis 
IBD
SLE
213
Q

How does anterior uveitis present?

A 
Dull progressive periocular pain 
Ocular hyperaemia 
Photophobia 
Blurry vision 
Increased lacrimation 
Hypopyon
214
Q

How is anterior uveitis investigated?

A

Slit lamp
Tonometry
Conjunctival smear

215
Q

How is anterior uveitis managed?

A

Glucocorticoids
Cycloplegics
Analgesia
Antibiotics/antiviral

216
Q

What is conjunctivitis?

A

Inflammation of the conjunctiva

217
Q

How does viral conjunctivitis present?

A 
Bilateral
Clear, watery discharge 
Normal vision
Conjunctival follicles 
FB Sensation 
Photophobia 
Discharge and crust 
Red eye
218
Q

How does bacterial conjunctivitis present?

A 
Unilateral 
Thick yellow purulent discharge 
Decrease in vision 
FB Sensation 
Photophobia 
Discharge and crust 
Red eye
219
Q

How does allergic conjunctivitis present?

A 
Itching 
Tearing 
Sneezing 
Ptosis 
FB Sensation 
Photophobia 
Discharge and crust 
Red eye
220
Q

Give 3 causes of viral conjunctivitis

A

Adenovirus
HSV
VZV

221
Q

Give 3 causes of bacterial conjunctivitis

A

Staph aureus
Strep pneumoniae
H influenzae
Pseudomonas

222
Q

What type of hypersensitivity reaction is allergic conjunctivitis?

A

Ig-E mediated

Type 1

223
Q

How is bacterial conjunctivitis managed?

A

Topical broad spectrum antibiotic

224
Q

How is viral conjunctivitis managed?

A

Topical antiviral

Cold compress

225
Q

How is allergic conjunctivitis managed?

A

Avoid triggers
Cold compress
Antihistamines
Corticosteroids

226
Q

What is episcleritis?

A

Inflammation of the superficial, episcleral layer of the eye

227
Q

Give 3 clinical features of episcleritis

A 
Acute onset red eye 
Discomfort 
Aching 
FB sensation 
Watering 
Photophobia 
Recurring episodes 
Normal vision
228
Q

Give 3 associated conditions with episcleritis

A 
UC 
Crohns
RA
Polyarteritis nodosa 
SLE
Wegener's 
Thyroid eye disease
229
Q

How is episcleritis managed?

A

Artificial tears
NSAIDs
Review in 1 week
(Self-limiting in 1-2 weeks)

230
Q

What is scleritis?

A

Inflammation of the full thickness of the sclera

231
Q

Give 3 associated conditions with scleritis

A 
RA 
Granulomatosis 
SLE
Ankylosing spondylitis
Gout
232
Q

Give 3 clinical features of scleritis

A 
Gradual onset 
Severe boring eye pain 
Radiates to neck and jaw 
Worse at night and on eye movements 
Watering 
Photophobia 
Decrease in vision 
Diplopia 
Tender globe
233
Q

How is scleritis managed?

A

Oral NSAIDs
Immunotherapy= Methotrexate, Azathioprine
Biological therapy= Infliximab

234
Q

Explain the pathophysiology of pre-proliferative diabetic retinopathy

A

Hyperglycemia causes the capillary walls in the eye to become weak and so microaneurysms form. The microaneurysms burst and form haemorrhages deep in the retina called Dot and Blot haemorrhages.

The weak vessels are also leaky which can collect under the macula and cause macular oedema. This results in visual loss. As the fluid dries it leaves behind hard exudates.

Over time the vessels become obstructed which causes infarction in the nerve fibre layer which presents as cotton wool spots.

235
Q

Describe early, moderate and late fundoscopy findings in pre-proliferative diabetic retinopathy

A

Early= microaneurysms

Moderate= multiple microaneurysms, dot and blot haemorrhages, venous bleeding, cotton wool spots

Late= 4-2-1 rule
4- diffuse intraretinal haemorrhages and microaneurysms in all 4 quadrants
2- venous bleeding in 2 quadrants
1- intraretinal microvascular abnormalities in >1 quadrant

236
Q

What percentage of patients with severe pre-proliferative diabetic retinopathy will progress to proliferative diabetic retinopathy within a year?

A

75% within a year

237
Q

Describe the pathophysiology of proliferative diabetic retinopathy

A

Prolonged ischaemia of the retina results in VEGF release which stimulates new growth of blood vessels (Neovascularization)

The fibrovascular proliferation extends beyond the internal limiting membrane and into the retina and vitreous. Vessels are leaky, fragile and misdirected.

As the vitreous shrinks with age the vessels tear causing vitreous haemorrhage and vision loss.

Vessels can put tension on the retina and cause a retinal detachment which results in vision loss especially if the macula is involved.

The new vessels can leak and cause macular oedema

The new vessels can also grow into the anterior chamber which obstructs the trabecular meshwork causing acute glaucoma

238
Q

How often are diabetics screened for retinopathy?

A

Annually

Every 3 months when pregnant

239
Q

How is diabetic retinopathy investigated?

A 
HbA1c
Visual acuity 
Slit lamp 
IOP measurement- tonometry 
Gonioscopy 
Fundoscopy 
OCT
240
Q

How is pre-proliferative diabetic retinopathy managed?

A

Tight glucose control (HbA1c <7%)
Stop smoking
Manage BP
Laser therapy of microaneurysms

241
Q

How is proliferative diabetic retinopathy managed?

A 
Tight glucose control (HbA1c <7%) 
Stop smoking 
Manage BP 
Laser therapy of microaneurysms
Photocoagulation 
Vitrectomy (if retinal detachment)

Macular oedema= anti-VEGF injections, corticosteroids

4. Senior Block- Special Senses (4 decks)

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