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OPTOM > OPTOM 353A > Flashcards

OPTOM 353A Flashcards

1
Q

Pathology meaning

A

The study of suffering

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2
Q

What is pathology

A

The study of the cause, development, the structural and functional changes associated with a disease

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3
Q

What is a disease

A

A deviation from a normal phenotype that is evident from subjective experience or objective measurement made by someone else

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4
Q

What is Etiology

A

Initial cause of a disease

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5
Q

What is Pathogenesis

A

The mechanism which an etiological factor causes disease

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6
Q

What is pathophysiology

A

Disturbance of normal physiological mechanisms that occur with the natural course of the disease

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7
Q

Sign vs Symptom

A

Sign is the manifestation of a disease a physician sees. A symptom is what the patient feels/sees

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8
Q

What is cause and effect

A

Where an action leads onto another

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9
Q

What is correlation

A

When one action is related to another action but does not cause each other

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10
Q

What is Glaucoma

A

Irreversible blindness that is not curable but can be slowed down to halt vision loss with treatment with early detection

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11
Q

Who does Glaucoma mainly affect

A

2-3% of people over 40

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12
Q

What is the consequence of glaucoma

A

Degenerative optic neuropathy, ONH changes which is associated with RGC death

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13
Q

What does RGC death cause

A

Visual field loss

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14
Q

How does reduced axoplasmic transport affect retinal fibre layer

A

optic nerve head damage which can be localised in the sup/inf area or very localised as a notch in the optic nerve head. This all gives visual field defects

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15
Q

Describe the fundus image reitnal fibre structure

A

The optic nerve begins in the retina at the retinal nerve fibre layer. The Horizontal raphe separate the superior and inferior of the optic nerve head that houses the superior and inferior arcuate bundles. There is also a Nasial radial bundle and a Papillomacular bundle.

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16
Q

Describe the cross section of the optic nerve head, with the layer names

A

In a cross section of the optic nerve head, there is the Pre-laminar, Laminar and the Post-laminar. The pre-laminar layer is the retinal layer. The Laminar is the layer that houses the Laminar cribrosa. The post-laminar is is everything else after the lamina cribrosa. In the cross section you will also see the central retinal artery with a thicker arterial wall and a central retinal vein. There is also the presence of the Pial, Arachnoid and Dura mater.

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17
Q

How does Glaucoma begin

A

rim loss and cup enlargement hence a larger C/D ratio, the lamina cribrosa thins and is displaced posteriorly, this results in the disrupted axonal transport to and from the LGN. Hence vision loss

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18
Q

What is axonal transport

A

Two way communication between RGC bodies and their synaptic terminals via microtubules and neurofilaments within axons

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19
Q

2 types of axonal transport

A

Anterograde and Retrograde

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20
Q

What is Anterograde transport

A

Delivers proteins and lipids

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21
Q

What is Retrograde tansport

A

For trophic factors for cell proliferation and differenction

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22
Q

What happens if axonal transport is reduced

A

RGC dysfunction and death

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23
Q

Characteristucs of a healthy NRR and optic cup

A

Thick and pink, Small optic cup and normal lamina cribrosa

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24
Q

Characteristics of thinning and cupping NRR and optic cup

A

Thin, atrophic and pale, large and deep optic cup and a distorted lamina cribrosa

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25
Q

What occurs in advanced glaucoma

A

Floor effect

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26
Q

What is the floor effect

A

Where with time and imaging, there is no durther structural changes in the optic nerve head and also major loss in all quadrants in visual field

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27
Q

3 theories on Glaucoma pathogenesis

A

Mechanical, Vascular/ischemic and Neurotoxicity theory

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28
Q

Mechanical theory of Glaucoma

A

High IOP compresses lamina cribrosa and fenestations become misaligned, the nerve fibres get compressed and the Retrograde axoplasmic flow of neutrophin is prevented. This results in RGCs apoptosis.

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29
Q

Vascular/Ischemic theory

A

Low perfusion at ONH giving ischemia resulting in lamina cribrosia degeneration. Retrograde axoplasmic flow of neutrophin prevented giving RGC apoptosis

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30
Q

Neurotoxicity Theory on glaucoma

A

Excess glutamate over stimulates neruons releasing too much intracellular Ca2+ which released anti-inflammatory and neurotoxic factors. This gives RGC apoptosis

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31
Q

Two Glaucoma Etiology

A

Primary and Secondary

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32
Q

Name types of primary glaucoma

A

Congenital, Open angle and Closed angle

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33
Q

Types of Open angle glaucoma

A

POAG form high IOP and Normal tension glaucoma

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34
Q

Types of closed angle glaucoma

A

Chronic, Acute and Intermittent

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35
Q

How does secondary glaucoma occur

A

Inflammatory, steroid, neovascular and traumatic

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36
Q

Aqueous drainage pathway

A

Post. Chamber –> Thru pupil –> Ant. Chamber –> Exit Ant. Chamber via Primary or Secondary drainage

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37
Q

What is primary drainage

A

Through TM and SC ( 90% )

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38
Q

What is secondary drainage

A

Through uveoscleral pathway ( 10% )

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39
Q

Glaucoma triad

A

> 21mmHg Ocular hypertension, Changes to RNFL/ONH, VF changes

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40
Q

Primary open angle glaucoma symptoms

A

Glaucoma triad + Not identifiable cause for high IOP and Open anterior chamber angle

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41
Q

Prumary open angle glaucoma risk factors

A

Black race, older age, elevated IOP, Thinner cornea, Myopia, Low diastolic perfusion pressure and Family history of POAG

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42
Q

Primary open angle glaucoma pathophysiology

A

Common in NZ, chronic and progressive, bilateral and asymmetric, reduce AH outflow from TM abnormalities

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43
Q

What is a variation of primary open angle glaucoma

A

Normal tension glaucoma

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44
Q

What is normal tension glaucoma

A

IOP consistently lower than 21mmHg with ONH damage and VF defects

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45
Q

What does ocular hyper tension and changes in VF indicate

A

Not glaucoma

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46
Q

What does ocular hypertension and changes to RNFL/ONH indicate

A

Pre-perimetric glaucoma

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47
Q

What is Primary angle closure glaucoma

A

Occlusion of TM by peripheral iris that obstructs outflow of AH giving high IOP

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48
Q

What kind of eye gets Angle closure more

A

Hyperopic eyes

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49
Q

Which race gets angle closure more

A

East asians

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50
Q

Two types of Primary angle closure mechanisms

A

Relative pupillary block and Non-pupillary block

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51
Q

What is relative pupillary block

A

Irido-lenticular contact forming seal so AH cant flow out so gives anterior bowing of the iris leading to irido-trabecular contact giving angle closure

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52
Q

WHat is non-pupillary block

A

In east asians due to iris configuration, thick or anteriorly positioned iris. This displaces the peripheral iris anteriorly giving iridotrabecular contact giving angle closure

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53
Q

Acute angle closure symptoms

A

Painful, vomitting, Poor vision, >50mmHg IOP, corneal oedema, shallow Ant. chamber and mid-dilated vertically oval pupil

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54
Q

What is a another risk for acute angle closure

A

Mydriasis when pupils are dilated

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55
Q

What are secondary Glaucomas

A

Results from pre-existing condition which can be open or closed angle

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56
Q

What is pigment dispersion syndrome

A

Known as PDS, it is mechanical rubbing of the iris pigmented epithelium against the zonules from excessive posterior bowing of the mid peripheral iris

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57
Q

Where do the pigments deposit on in PDS

A

Through out Anterior chamber, TM, corneal endothelium and anterior lens

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58
Q

Who is affected by PDS and what does it lead to

A

2-4% young myopic adults, caucasians and males. It leads to pigmentary glaucoma

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59
Q

What is pseudoexfoliative syndrome

A

Pseudoexfoliative materia in the eye and is deposited onto the TM, COrnea, Anterior lens, iris and lens zonules

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60
Q

What happens if the pseudoexfoliate is deposited onto these structures

A

TM gives bad AH outflow giving higher IOP

On the cornea will show pigments sattered on the endothelium

On the anteroir lens can be seen with pupil dilation

On the iris can be seen by transillumination at the pupil ruff

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61
Q

Who gets pseudoexfoliative syndrome and what does it lead to

A

In women, usually bilateral and linked to the LOXL1 gene. Results in pseudoexfoliative glaucoma

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62
Q

What is neovascular glaucoma

A

From severe and chronic retinal ischemia such as central retinal vein occlusion. Ischemia released VEGF which diffuses into the anterior chamber giving iris neovascularisation. Vessels grow towards angle and invades TM reducing AH outflow and increases IOP

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63
Q

What is inflammatory glaucoma

A

From Uveitis where the worse the uveitis, the higher chance of glaucoma

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64
Q

Types of inflammatory glaucoma

A

Secondary open angle, Secondary angle closure with and without pupillary block

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65
Q

How does secondary open angle glaucoma occur

A

Inflamm increases IOP, inflamm cells deposit onto TM decreasing AH outflow and increases IOP

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66
Q

How does secondary agle closure without pupillary block occur

A

Inflamm cells deposit in angle, contracts peripheral iris over the TM giving peripheral anterior synechaie resulting in angle closure

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67
Q

How does Secondary angle closure with pupillary block occur

A

Inflamm cells encourage posterior synechaie giving iris bowing resulting in peripheral anterior synechaie resulting in angle closure

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68
Q

Lens related glaucoma

A

Produces phacomorphic glaucoma and Phacolytic glaucoma

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69
Q

What is phacomorphic glaucoma

A

Anterior lens growth giving posterior synechiae resulting in pupil block

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70
Q

What is phacolytic glaucoma

A

proteins leak through capsule, deposits onto TM… and involves a hypermature cataractous lens

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71
Q

Steroid induced glaucoma

A

Occurs secondary to corticosteroid induced raised IOP. Has higher, moderate and non-responders

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72
Q

Describe the higher, moderate and non-responders to IOP in steroid induced glaucoma

A

Higher responders = IOP increase more than 15mmHg

Moderate responders = IOP increase between 6-16mmHg

Non-responders = IOP increase less than 6mmHg

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73
Q

Congenital Glaucoma

A

Can be primary or secondary. This has an underdeveloped anterior chamber angle that affects AH outflow. Can be sporadic or autosomal recessive

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74
Q

Symptoms of congenitial glaucoma

A

Higher IOP stretches eye causing slcera to be blueish, also a Haab Striae in the descements membrane. ONH cupping can regress and even reverse

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75
Q

Peters Anomaly

A

defective neural crest cell migration during development. Is sporadic but can be autosomal recessive inherited

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76
Q

Types of peters anomaly

A

Type 1, 2 and peters plus syndrome

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77
Q

What is Type 1 peters anomaly

A

affects cornea only

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78
Q

What is type 2 peters anomaly

A

Affects cornea and the lens

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79
Q

What is peters plus syndrome in peters anomaly

A

Has systemic abnormalities, onset in infancy and glaucoma occurs in 50% of Peters Anomaly cases due to anterior chamber angle abnormalities

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80
Q

Axenfeld-Rieger Syndrome types

A

Axenfeld Anomaly, Rieger Anomaly and Riger Syndrome

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81
Q

What is Axenfeld anomaly

A

Posterior Embryotoxon

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82
Q

What is riegers anomaly

A

Iris anomalies

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83
Q

What is Rieger syndrome

A

Rieger anomaly with bone, facial and dental defects

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84
Q

Chances of glaucoma in Axenfeld-rieger syndrome

A

50% of Axenfeld-rieger syndrome cases due to anterior chamber abnormalities

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85
Q

ONH exam observations

A

C/D ratio, ONH size, NRR, Vasculature changes and Laminar Dot sign

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86
Q

What to observe in C/D ratio

A

Irreversible decrease in nerve fibres, glial cells ad blood vessels. Higher C/D ratio is significant, also observe for C/D ratio asymmetry between eyes of more than 0.2 is suspicious

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87
Q

Observations in ONH size

A

Larger cupping in larger ONH may be physiological rathee than pathological. A C/D ratio symmetry is explained if the eyes have different ONH sizes. Small disc is 1.1-1.3mm and Larger disc is more than 1.8mm

88
Q

NRR observations

A

Must follow ISNT rule where the inferior cup is thicker than the rest. Observe for notching in sup/inf areas

89
Q

Vasculature observations

A

Bayoneting of blood vessels indicate NRR erosion, also Drance haemorrhage is sign of glaucotamous ONH damage

90
Q

Laminar dot sign observation

A

Deep cupping with lamina pores visible occuring in advancing glaucoma. Seen as grey dots in lamina cribrosa from loss of RGC axons. Fenestrations also misaligned as lamina is distorted

91
Q

Why RNFL exam is important

A

Not only in glaucoma, also i nother diseases too. But in Glaucoma, RNFL defects always found with detectable ONH changes

92
Q

What can OCT see

A

Structural damages in glaucoma and gives assessment of ONH size, C/D ratio, NRR and RNFL thickness. But cant be used as standalone screening tool

93
Q

What is gold standard for measuring VF

A

Humphrey visual field analyser

94
Q

How does the Humphrey visual field analyser work

A

Estimates threshold sensitivity within px VF and is central 24-30 degrees. Stimulus differences like size, colour and type

95
Q

What is tonometry

A

Measures IOP and different devices used for this

96
Q

What is gold standard for tonometry

A

Goldmann applanation tonometry

97
Q

What is tonometry affected by

A

Central corneal thickness, corneal curvature, corneal hydration and corneal structural integrity

98
Q

What does gonioscopy do

A

See anterior chamber angle strutures and differentiate between glaucoma types

99
Q

What does Pachymetry do

A

Measures Central corneal thickness

100
Q

Why is central corneal thickness relevant to glaucoma

A

It is an independent risk factor for primary open angle glaucoma

101
Q

What thickness of the cornea makes the goldmann applanation tonometry most accurate

A

520um

102
Q

What happens to IOP measurement if cornea is thicker

A

Over estimates IOP

103
Q

What visual tests can be done to test for glaucoma visual function

A

pupil reactions and colour vision, glaucoma affects this

104
Q

Glaucoma history taking includes

A

px ocular history, refractive error, any eye disease history, any surgery doen and inflammation. General health includes any systemic diseases, current/previous medication. Also find any family history of glaucoma

105
Q

What is the aim in glaucoma management

A

Lower IOP to levels that prevents any further damage to the optic nerve head.

106
Q

What is the only modifiable risk factor in glaucoma

A

IOP

107
Q

When were optometrists allowed to do glaucoma management

A

2014

108
Q

What is IOP determined by

A

Balance of inflow and outflow of AH which varies with time of day, heartbeat, blood pressure and respiration.

109
Q

When do IOP fluctuations occur most

A

Higher in mornings and lower in the afternoon

110
Q

How much more chance to get glaucoma with increasing IOP

A

10% chance per 1mmHg

111
Q

What is another significant risk factor for glaucoma between two eyes

A

If the IOP different between two eyes is more than 6mmHg

112
Q

AH production depend on?

A

Combo of active and passive secretion

113
Q

AH turnover rate

A

2 uL/m

114
Q

Where is AH produced and the structure of the ciliary process

A

Produced in the ciliary processes within the pars plicata. NPE faces AH and PE faces ciliary process in the stroma

115
Q

How many steps in AH production and what are they

A

Diffusion, Ultrafiltration and active secretion

116
Q

How much of AH is actively secreted

A

80-90%

117
Q

How is AH secreted

A

Blood enters capillaries, plasma foes into ciliary stroma and then the ciliary epithelium actively pumps the plasma components into the posterior chamber resulting in AH. Secretion starts from Stroma –> PE –> NPE then Posterior chamber as AH

118
Q

How to increase AH drainage

A

Prostaglandin analoues and Muscarinic agonists

119
Q

How to decrease AH production

A

Carbonic anhydrase inhibitors and beta blockers

120
Q

How to induce both increase in AH drainage and decrease in AH production

A

alpha agonists

121
Q

Types of non-medical management for AH

A

Laser and Surgery

122
Q

Laser AH management

A

Laser trbeculoplasty and Laser peripheral iridotmy

123
Q

Surgery AH management

A

Peripheral iridectomy, Minimally invasive glaucoma surgery, trabeculectomy, cyclodestructive procedures like photocoagulation

124
Q

What is optic neuropathy

A

Optic nerve damage of any cause, can be congenital or Acquired

125
Q

Types of Acquired optic neuropathies

A

Papilloedema, optic neuritis, anterior ischemic optic neuropathy and optic nerve head tumors

126
Q

Types of Congenital optic neuropathies

A

Hereditary, like optic disc coloboma, optic disc pit, morning glory disc and tilted disc syndrome

127
Q

What is ONH coloboma

A

Missing section of the ONH at birth seen as a glistening white bowl shaped excavation within the ONH, can be uni or bilateral and is infero-nasal.

128
Q

How is ONH coloboma caused

A

Incomplete closure of embryonic optic fissure and the condition is mostly sporadic and can be inherited from AD or PAX6 gene

129
Q

What is an ONH pit

A

Localised hole in optic disc at birth, it is a round/oval depression within ONH and is temporal or central. This can lead to macolopathy where fluid accummulation gives macular oedema and visual defects

130
Q

What is morning glory disc

A

Congenital excavation of the posterior globe surrounding and involves the ONH. This is seen as an enlarged and orange/pink ONH with a funnel shaped excavation.

131
Q

What causes Morning glory disc

A

Either abnormal formation of the posterior sclera and the lamina cribrosa or the sedondary herniation of neural tissue through the defect. COmmon in females and associated with conditions like MG

132
Q

What is tilted disc syndrome

A

Known as Fuch’s coloboma, it is congenital where the ONH appears oblique. The ONH also transposes inferno-nasally due to the angled entry of the optic nerve into the globe

133
Q

Effects of a tilted disc

A

Increase chances of myopia and astigmatism

134
Q

What is Optic Disc Hypoplasia

A

Common congenital anomaly where there is decreased number of nerve axons wihtin normal glial tissue

135
Q

Observations in Optic Disc Hypoplasia

A

ONH is smal and pale, also the optic nerve being underdeveloped during gestation is associated with CNS or pituitary abnormalities

136
Q

What is optic disc medullation

A

Abnormal RNFL anterior to lamina cribrosa. Has opqaue patches with feathery edges that is contiguous to the ONH and unilateral.

137
Q

Effects of optic disc medullation

A

Cause oligodendrocytes to migrate and different to continue myelination which is associated with Down syndrome, turners syndrome and epilepsy

138
Q

What are ONH drusens

A

Acellular concretions anterior to the lamina cribrosa where whitish-yellow, round crystalline deposits are embedded within the ONH. And found in caucasions

139
Q

What papilloedema

A

ONH swelling, exclusively secondary to raised intra-cranial pressure where the the pressure from the intra-craniel pressure to the subarachnoid space surrounding the optic nerve hinders anterograde axoplasmic flow in RGC axons

140
Q

How does elevated intra-craniel pressure arise

A

Intra-cranial lesions, cerebral oedemas from blunt head trauma and the impairment of CSF absorption

141
Q

Stages of papilloedema

A

Early –> Acute –> Chronic –> Atrophic

142
Q

Early Papilloedema

A

Mild ONH hyperaemia where optic cup is preserved and has indistinct ONH margins and peripapillary RNFL striations

143
Q

Acute Papilloedema

A

Servere ONH hyperaemia, absence of cup with larger ONH, Vacular congestion
( Venous engorgement, Peripapillary flame haemorrhages and cotton wool spots ), there is finally mechanical deformation known as Paton lines

144
Q

Chronic Papilloedema

A

Severe ONH hyperaemia, absence of cup with larger ONH, Vascular congestion
( Venous engorgement and Optociliary shunts ), Hard exudates known as Corpora Amylacea

145
Q

Atrophic Papilloedema

A

Subsided ONH swelling with NRR pallor and narrowed retinal arterioles

146
Q

What is psuedotumour cerebri

A

AKA ( Idiopathic intracraniel hypertension ), which is a papilloedema caused by raised ICP with no identifiable cause and common in px less than 50, common in overweight women of productive age

147
Q

What is optic neuritis

A

Diverse group for inflammatory optic nerve diseases caused by demyelination of optic nerve neurons leading to axonal injury and apoptosis

148
Q

Etiologies of optic neuritis

A

Atypical or Typical

149
Q

Atypical optic neuritis

A

From infection of autoimmune

150
Q

Typical optic neuritis

A

Usually idiopathic or a demyelinating lesion like MS

151
Q

What is the optic neuropathy triad

A

Vision loss, periocular pain and dychromatopsia

152
Q

Three types of otpic nerve damage

A

Retrobulbar neuritis, Papillitis, Neuroetinitis

153
Q

What is retrobulbar neuritis

A

2/3 Optic nerve cases where ONH appears normal but thats due to the inflammation is posterior to the globe

154
Q

What is papillitis

A

Inflammation of the ONH, ONH hyperaemia, oedema and peripapillary flame haems

155
Q

What is neurotinitis

A

Papilliis with inflammation of the RNFL and a Macular star

156
Q

What is MS

A

chronic demyelinating and neurodegenerative disease of the CNS where scarring forms in response to demyelination leading to neurological dysfunction and disability over time

157
Q

Who is affected by MS and the consequence of MS

A

Young individuals, female more likely.

Half of MS px will have optic neuropathy and half of px with neuropathy will get MS within 15 years. A landmark in the brain scans are is the Dawsons finger

158
Q

What does AION stand for

A

Anterior ischaemic optic neuropathy

159
Q

What is anterior ischemic optic neuropathy

A

an occlusion of the sPCAs blood flow giving partial or total infarction of the ONH. It is seen in the 1mm anterior intraocular portion of the optic nerve

160
Q

Two classifications of AION - Anterior ischemic optic neuropathy

A

Arteritic AION and Non-arteritic AION

161
Q

What is Arteritic AION

A

NEURO-OPHTHALMIC EMERGENCY.

The inflammation of the sPCA gives thrombotic occlusion. If inflamed medium and large arteries are untreated, it will lead to Arteritic-Anterior-Ischemic-Optic-Neuropathy.

162
Q

Arteritic AION symptoms

A

Temporal headache, Jaw Claudification, fevers, proximal muscle pain and stiffness. Diplopia also seen

163
Q

WHat is Non-Arteritic AION

A

Common form of ischemic optic neuropathy which does not involve inflammation of vessels. There is sudden and painless vision loss upon waking up. affecting people under 50 with equal M:F gender ratio.

164
Q

Non-arteritic AION systemic associations

A

Hyperlipidemia and atherosclerotic diseases like angina and stroke

165
Q

Non-arteritic AION ocular associations

A

Disc and risk in the fellow eye

166
Q

What is Age related Macular Degeneration ( AMD )

A

Common irreversible blindness associated with Macular Drusen at the bruchs membrane

167
Q

Who does AMD effect

A

Older caucasions over 65

168
Q

AMD progression and where does it affect

A

Slow and affects central vision

169
Q

How to detect AMD

A

using Amsler grid

170
Q

What does macular drusen look like

A

Like the surface of the sun around the macular

171
Q

AMD risk factors

A

Age, lighter iris colour, smoking, UV and higher BMI

172
Q

How does smoking cause AMD

A

Increases AMD severity and lowers antioxidants

173
Q

What can reduce AMD

A

Red wine, green vegetables and vitamin supplements

174
Q

Why does AMD have central vision loss

A

High density of photoreeptors needing high oxygen demand, not enough oxygen

175
Q

What is the only blood supply to the central retina

A

The choroid

176
Q

What happens to blood supply in the retina with age and its effects

A

Decreases choriocapillaris density and lumen diameter which decreases blood flow so oxidative damage increased to ocular tissue

177
Q

Where is Macular drusen found

A

Between bruchs membrane and the RPE

178
Q

Where is the RPE

A

Single layer between Bruchs membrane and photoreceptors

179
Q

Function of the RPE

A

Phagocytosis of the photoreceptors outer segments and forms tight junction between RPE cells forming the blood retinal barrrier, also absorbs light and gives nutrients to photoreceptors, active transport of metabolites and finally recycles/stores visual pigment

180
Q

When are rods and cones phagocytosed

A

Rods in the morning and Cones in the evening

181
Q

Causes of AMD

A

Lipofuscin deposits, Oxidative stress, reduced choroidal blood flow and chronic inflammation

182
Q

How does lipofuscin cause AMD

A

It is a waste product from digested outer segment of photoreceptors and this accumulates with age. Light causes lipofuscin to form ROS which is toxic to the RPE, RPE damaged cannot clear waste and cannot nourish photoreceptors so it dies

183
Q

How do changes in the choroid cause AMD

A

Choroid thins with age, has choroidal vascular depletion in early AMD and progresses. There is also an accumulation of membrane attack complexes inthe choriocapillaris in AMD, as well as mast cell and macrophage activation

184
Q

How does Chronic inflammation cause AMD

A

Inflammation is caused from the debris that cuases drusen formation. The debris also introduces inflammatory meditators from the RPE and choroid which all give chronic inflammatory response

185
Q

Two types of AMD

A

Atrophic ( Dry ) and Exudative ( Wet )

186
Q

What is atrophic AMD

A

90% cases, has drusen progressing into Grographic atrophy of the macular and reduced vision

187
Q

What is exudative AMD

A

10% cases, responsible for 90% of severe vision loss associated with AMD. This has soft drusen and RPE detechment + Haemorrhage from subretinal neovescularisation.

Choroidal neovascularisation results in ischemic tissues releasing angiogenic factor VEGF

188
Q

Treatment for atrophic AMD

A

Monthly intravitreal injections of pegcetacoplan which slows geographic atrophy but increased chances of conjunctival hemorrhage with increased IOP and blurred vision

189
Q

Treatment for Exudative AMD

A

Thermal laser photocoagulation to seal blood vessels, photodynamic therapy where compound is laser activated injected into blood stream damaging new vessel endothelial cells. And Anti-VEGF therapy where VEGF inhibitor like Avastin is injected into the vitreous every month

190
Q

Current statistics and characteristics for myopia

A

Almost all human myopia is axial and mostly in Asian countries. Also have increased amount of myopia in recent decades, so eye size and refractive error is not just genetics

191
Q

What does myopia depend on

A

Genetics and Environment

192
Q

Consequence of eye elongation in myopia

A

This is a scleral abnormality. Here the retina and the choroid are stretched and becomes thinner and damaged resulting in myopic maculopathy

193
Q

Classification of myopia

A

Mild myopia –> Less than -3.00D

Moderate Myopia –> -3.00D - -6.00D

High myopia –> more than -6.00D

194
Q

Other health risks in having myopia

A

Increased risk of glaucoma and cataracts. It is also associated with an increased risk of pathology

195
Q

What does increasing myopia mean for the patient

A

Increased risk for Myopic Maculopathy and retinal detachment

196
Q

Explain the onset of Myopia

A

Occurs in childhood and progresses and stabilises around the 20 years of age

197
Q

Describe the fundus changes seen in Myopia

A

Optic disc crescent, Tessellated fundus

These below are sight threatening changes,
Posterior Staphyloma, Chorioretinal Atrophy either diffuse or patchy, Lacquer cracks, Fuch’s spot and Retinoschesis

198
Q

What is observed in optic disc crescent

A

Usually on the temporal side of disc

199
Q

What is observed in Tessellated Fundus

A

Choroidal vessels visible due to hypoplasia of RPE cells

200
Q

What is observed in staphyloma and chorioretinal atrophy

A

Bulging of the temporal walls in the orbit in an MRI scan

Arcuate vasculature becomes straightened

201
Q

What is observed in Lacquer cracks in Myopia

A

Breaks in the Bruch’s membrane due to it stretching as the eye enlarges, it is seen as a fine irregular yellow line on the fundus

There is also poor future prognosis for central vision

202
Q

What is observed in Fuch’s spot

A

Occurs with Foveal Choroidal Neovascularisation and haemorrhage that leaves scars and a central scotoma in their vision

203
Q

What is Macular Retinoschesis in high myopia

A

The splitting of the layers of the retina

The inner retina adheres to the tight inner limiting membrane and is separated from the outer retina that adheres to the choroid which expands with progressing myopia

204
Q

Describe the 4 Treatments for slowing myopia progression and how they work

A

Optical treatments creating myopic defocus on the retina with MiSight contact lenses and Mypoia control spectacles

Atropine eyedrops has an anti-myopia effect but mode of action unknown

Red laser light therapy appears to be very effective but unknown long term safety

Reducing myopia INCIDENCE such as increased out-door time in children

205
Q

Describe Central Serous Retinopathy and its characteristics

A

Common in middled aged Type A males, Has a local retinal detachment over a local accumulation of fluid with or without RPE detachment and has a local scotoma

Can be associated with long term visual effects and this regresses within months spontaneously

206
Q

What is a type A personality

A

Job involvement, competitiveness and impatience

207
Q

What is a Cystoid Macular Edema ( CME / CMO )`

A

Fluid-filled microcysts in the retina which can coalesce into larger cysts

These cysts can break through to form macular holes

208
Q

Cystoid Macular Edema Etiologies

A

Diabetic neuropathy, Uveitis, Idiopathic and Retinitis Pigmentosa

209
Q

Causes of Macular holes

A

Traction of the perifoveal vitreous, Associated with staphyloma giving retinal detachment in high myopes, Trauma giving cystoid macular oedema resulting in macular hole, Solar retinopathy and Idiopathic in post-menopausal women

210
Q

What does an Epiretinal membrane look like

A

From fine, glistening membrane overlying the macula to thick and white tissue obscuring the retinal bvs which may cause traction and retinal pucker

211
Q

Characteristics of Epiretinal membranes

A

Common in people over 50 where early stage is asymptomatic and decreases VA

Progression gives metamorphopsia and has severe decrease in VA

Break in Inner limiting membrane allows the escape and proliferation of glial cells which form a membrane along the surface of the ILM forming a membrane

In older px, this is related to PVD

212
Q

Name the two Toxic Maculopathies

A

Chloroquine and Tamoxifen Maculopathy

213
Q

Chloroquine maculopathy

A

Plaquenil used to treat malaria, rheumatoid arthritis and plus erythematosis

The drug has an affinity for melanin so its concentrated in the eye and damages lysozomes, RPE and Photoreceptors

This continues for years after ingestion leading to retinopathy progression

214
Q

Tamoxifen Maculopathy

A

Tamoxifen is an estrogen antagonist and binds to estrogen receptors on breast cancer cells, and decreases DNA synthesis

This drug is toxic at high dosage which is revesible, has crystalline retinopathy with cystoid macular edemas and finally causes Optic neuritis

215
Q

What is Thiazolidinediones ( TZDs )

A

A drug for glycemic control for diabetes, these act as insulin sensitisers to reduce glucose, fatty acids and insulin blood concentration

Two drugs known as Avandia and Actos

216
Q

What is the side effect of Thiazolidinediones

A

Macula Edema

217
Q
A

OPTOM (6 decks)

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