OPTOM 353A Flashcards
Pathology meaning
The study of suffering
What is pathology
The study of the cause, development, the structural and functional changes associated with a disease
What is a disease
A deviation from a normal phenotype that is evident from subjective experience or objective measurement made by someone else
What is Etiology
Initial cause of a disease
What is Pathogenesis
The mechanism which an etiological factor causes disease
What is pathophysiology
Disturbance of normal physiological mechanisms that occur with the natural course of the disease
Sign vs Symptom
Sign is the manifestation of a disease a physician sees. A symptom is what the patient feels/sees
What is cause and effect
Where an action leads onto another
What is correlation
When one action is related to another action but does not cause each other
What is Glaucoma
Irreversible blindness that is not curable but can be slowed down to halt vision loss with treatment with early detection
Who does Glaucoma mainly affect
2-3% of people over 40
What is the consequence of glaucoma
Degenerative optic neuropathy, ONH changes which is associated with RGC death
What does RGC death cause
Visual field loss
How does reduced axoplasmic transport affect retinal fibre layer
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
Describe the fundus image reitnal fibre structure
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.
Describe the cross section of the optic nerve head, with the layer names
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.
How does Glaucoma begin
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
What is axonal transport
Two way communication between RGC bodies and their synaptic terminals via microtubules and neurofilaments within axons
2 types of axonal transport
Anterograde and Retrograde
What is Anterograde transport
Delivers proteins and lipids
What is Retrograde tansport
For trophic factors for cell proliferation and differenction
What happens if axonal transport is reduced
RGC dysfunction and death
Characteristucs of a healthy NRR and optic cup
Thick and pink, Small optic cup and normal lamina cribrosa
Characteristics of thinning and cupping NRR and optic cup
Thin, atrophic and pale, large and deep optic cup and a distorted lamina cribrosa
What occurs in advanced glaucoma
Floor effect
What is the floor effect
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
3 theories on Glaucoma pathogenesis
Mechanical, Vascular/ischemic and Neurotoxicity theory
Mechanical theory of Glaucoma
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.
Vascular/Ischemic theory
Low perfusion at ONH giving ischemia resulting in lamina cribrosia degeneration. Retrograde axoplasmic flow of neutrophin prevented giving RGC apoptosis
Neurotoxicity Theory on glaucoma
Excess glutamate over stimulates neruons releasing too much intracellular Ca2+ which released anti-inflammatory and neurotoxic factors. This gives RGC apoptosis
Two Glaucoma Etiology
Primary and Secondary
Name types of primary glaucoma
Congenital, Open angle and Closed angle
Types of Open angle glaucoma
POAG form high IOP and Normal tension glaucoma
Types of closed angle glaucoma
Chronic, Acute and Intermittent
How does secondary glaucoma occur
Inflammatory, steroid, neovascular and traumatic
Aqueous drainage pathway
Post. Chamber –> Thru pupil –> Ant. Chamber –> Exit Ant. Chamber via Primary or Secondary drainage
What is primary drainage
Through TM and SC ( 90% )
What is secondary drainage
Through uveoscleral pathway ( 10% )
Glaucoma triad
> 21mmHg Ocular hypertension, Changes to RNFL/ONH, VF changes
Primary open angle glaucoma symptoms
Glaucoma triad + Not identifiable cause for high IOP and Open anterior chamber angle
Prumary open angle glaucoma risk factors
Black race, older age, elevated IOP, Thinner cornea, Myopia, Low diastolic perfusion pressure and Family history of POAG
Primary open angle glaucoma pathophysiology
Common in NZ, chronic and progressive, bilateral and asymmetric, reduce AH outflow from TM abnormalities
What is a variation of primary open angle glaucoma
Normal tension glaucoma
What is normal tension glaucoma
IOP consistently lower than 21mmHg with ONH damage and VF defects
What does ocular hyper tension and changes in VF indicate
Not glaucoma
What does ocular hypertension and changes to RNFL/ONH indicate
Pre-perimetric glaucoma
What is Primary angle closure glaucoma
Occlusion of TM by peripheral iris that obstructs outflow of AH giving high IOP
What kind of eye gets Angle closure more
Hyperopic eyes
Which race gets angle closure more
East asians
Two types of Primary angle closure mechanisms
Relative pupillary block and Non-pupillary block
What is relative pupillary block
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
WHat is non-pupillary block
In east asians due to iris configuration, thick or anteriorly positioned iris. This displaces the peripheral iris anteriorly giving iridotrabecular contact giving angle closure
Acute angle closure symptoms
Painful, vomitting, Poor vision, >50mmHg IOP, corneal oedema, shallow Ant. chamber and mid-dilated vertically oval pupil
What is a another risk for acute angle closure
Mydriasis when pupils are dilated
What are secondary Glaucomas
Results from pre-existing condition which can be open or closed angle
What is pigment dispersion syndrome
Known as PDS, it is mechanical rubbing of the iris pigmented epithelium against the zonules from excessive posterior bowing of the mid peripheral iris
Where do the pigments deposit on in PDS
Through out Anterior chamber, TM, corneal endothelium and anterior lens
Who is affected by PDS and what does it lead to
2-4% young myopic adults, caucasians and males. It leads to pigmentary glaucoma
What is pseudoexfoliative syndrome
Pseudoexfoliative materia in the eye and is deposited onto the TM, COrnea, Anterior lens, iris and lens zonules
What happens if the pseudoexfoliate is deposited onto these structures
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
Who gets pseudoexfoliative syndrome and what does it lead to
In women, usually bilateral and linked to the LOXL1 gene. Results in pseudoexfoliative glaucoma
What is neovascular glaucoma
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
What is inflammatory glaucoma
From Uveitis where the worse the uveitis, the higher chance of glaucoma
Types of inflammatory glaucoma
Secondary open angle, Secondary angle closure with and without pupillary block
How does secondary open angle glaucoma occur
Inflamm increases IOP, inflamm cells deposit onto TM decreasing AH outflow and increases IOP
How does secondary agle closure without pupillary block occur
Inflamm cells deposit in angle, contracts peripheral iris over the TM giving peripheral anterior synechaie resulting in angle closure
How does Secondary angle closure with pupillary block occur
Inflamm cells encourage posterior synechaie giving iris bowing resulting in peripheral anterior synechaie resulting in angle closure
Lens related glaucoma
Produces phacomorphic glaucoma and Phacolytic glaucoma
What is phacomorphic glaucoma
Anterior lens growth giving posterior synechiae resulting in pupil block
What is phacolytic glaucoma
proteins leak through capsule, deposits onto TM… and involves a hypermature cataractous lens
Steroid induced glaucoma
Occurs secondary to corticosteroid induced raised IOP. Has higher, moderate and non-responders
Describe the higher, moderate and non-responders to IOP in steroid induced glaucoma
Higher responders = IOP increase more than 15mmHg
Moderate responders = IOP increase between 6-16mmHg
Non-responders = IOP increase less than 6mmHg
Congenital Glaucoma
Can be primary or secondary. This has an underdeveloped anterior chamber angle that affects AH outflow. Can be sporadic or autosomal recessive
Symptoms of congenitial glaucoma
Higher IOP stretches eye causing slcera to be blueish, also a Haab Striae in the descements membrane. ONH cupping can regress and even reverse
Peters Anomaly
defective neural crest cell migration during development. Is sporadic but can be autosomal recessive inherited
Types of peters anomaly
Type 1, 2 and peters plus syndrome
What is Type 1 peters anomaly
affects cornea only
What is type 2 peters anomaly
Affects cornea and the lens
What is peters plus syndrome in peters anomaly
Has systemic abnormalities, onset in infancy and glaucoma occurs in 50% of Peters Anomaly cases due to anterior chamber angle abnormalities
Axenfeld-Rieger Syndrome types
Axenfeld Anomaly, Rieger Anomaly and Riger Syndrome
What is Axenfeld anomaly
Posterior Embryotoxon
What is riegers anomaly
Iris anomalies
What is Rieger syndrome
Rieger anomaly with bone, facial and dental defects
Chances of glaucoma in Axenfeld-rieger syndrome
50% of Axenfeld-rieger syndrome cases due to anterior chamber abnormalities
ONH exam observations
C/D ratio, ONH size, NRR, Vasculature changes and Laminar Dot sign
What to observe in C/D ratio
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
Observations in ONH size
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
NRR observations
Must follow ISNT rule where the inferior cup is thicker than the rest. Observe for notching in sup/inf areas
Vasculature observations
Bayoneting of blood vessels indicate NRR erosion, also Drance haemorrhage is sign of glaucotamous ONH damage
Laminar dot sign observation
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
Why RNFL exam is important
Not only in glaucoma, also i nother diseases too. But in Glaucoma, RNFL defects always found with detectable ONH changes
What can OCT see
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
What is gold standard for measuring VF
Humphrey visual field analyser
How does the Humphrey visual field analyser work
Estimates threshold sensitivity within px VF and is central 24-30 degrees. Stimulus differences like size, colour and type
What is tonometry
Measures IOP and different devices used for this
What is gold standard for tonometry
Goldmann applanation tonometry
What is tonometry affected by
Central corneal thickness, corneal curvature, corneal hydration and corneal structural integrity
What does gonioscopy do
See anterior chamber angle strutures and differentiate between glaucoma types
What does Pachymetry do
Measures Central corneal thickness
Why is central corneal thickness relevant to glaucoma
It is an independent risk factor for primary open angle glaucoma
What thickness of the cornea makes the goldmann applanation tonometry most accurate
520um
What happens to IOP measurement if cornea is thicker
Over estimates IOP
What visual tests can be done to test for glaucoma visual function
pupil reactions and colour vision, glaucoma affects this
Glaucoma history taking includes
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
What is the aim in glaucoma management
Lower IOP to levels that prevents any further damage to the optic nerve head.
What is the only modifiable risk factor in glaucoma
IOP
When were optometrists allowed to do glaucoma management
2014
What is IOP determined by
Balance of inflow and outflow of AH which varies with time of day, heartbeat, blood pressure and respiration.
When do IOP fluctuations occur most
Higher in mornings and lower in the afternoon
How much more chance to get glaucoma with increasing IOP
10% chance per 1mmHg
What is another significant risk factor for glaucoma between two eyes
If the IOP different between two eyes is more than 6mmHg
AH production depend on?
Combo of active and passive secretion
AH turnover rate
2 uL/m
Where is AH produced and the structure of the ciliary process
Produced in the ciliary processes within the pars plicata. NPE faces AH and PE faces ciliary process in the stroma
How many steps in AH production and what are they
Diffusion, Ultrafiltration and active secretion
How much of AH is actively secreted
80-90%
How is AH secreted
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
How to increase AH drainage
Prostaglandin analoues and Muscarinic agonists
How to decrease AH production
Carbonic anhydrase inhibitors and beta blockers
How to induce both increase in AH drainage and decrease in AH production
alpha agonists
Types of non-medical management for AH
Laser and Surgery
Laser AH management
Laser trbeculoplasty and Laser peripheral iridotmy
Surgery AH management
Peripheral iridectomy, Minimally invasive glaucoma surgery, trabeculectomy, cyclodestructive procedures like photocoagulation
What is optic neuropathy
Optic nerve damage of any cause, can be congenital or Acquired
Types of Acquired optic neuropathies
Papilloedema, optic neuritis, anterior ischemic optic neuropathy and optic nerve head tumors
Types of Congenital optic neuropathies
Hereditary, like optic disc coloboma, optic disc pit, morning glory disc and tilted disc syndrome
What is ONH coloboma
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.
How is ONH coloboma caused
Incomplete closure of embryonic optic fissure and the condition is mostly sporadic and can be inherited from AD or PAX6 gene
What is an ONH pit
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
What is morning glory disc
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.
What causes Morning glory disc
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
What is tilted disc syndrome
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
Effects of a tilted disc
Increase chances of myopia and astigmatism
What is Optic Disc Hypoplasia
Common congenital anomaly where there is decreased number of nerve axons wihtin normal glial tissue
Observations in Optic Disc Hypoplasia
ONH is smal and pale, also the optic nerve being underdeveloped during gestation is associated with CNS or pituitary abnormalities
What is optic disc medullation
Abnormal RNFL anterior to lamina cribrosa. Has opqaue patches with feathery edges that is contiguous to the ONH and unilateral.
Effects of optic disc medullation
Cause oligodendrocytes to migrate and different to continue myelination which is associated with Down syndrome, turners syndrome and epilepsy
What are ONH drusens
Acellular concretions anterior to the lamina cribrosa where whitish-yellow, round crystalline deposits are embedded within the ONH. And found in caucasions
What papilloedema
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
How does elevated intra-craniel pressure arise
Intra-cranial lesions, cerebral oedemas from blunt head trauma and the impairment of CSF absorption
Stages of papilloedema
Early –> Acute –> Chronic –> Atrophic
Early Papilloedema
Mild ONH hyperaemia where optic cup is preserved and has indistinct ONH margins and peripapillary RNFL striations
Acute Papilloedema
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
Chronic Papilloedema
Severe ONH hyperaemia, absence of cup with larger ONH, Vascular congestion
( Venous engorgement and Optociliary shunts ), Hard exudates known as Corpora Amylacea
Atrophic Papilloedema
Subsided ONH swelling with NRR pallor and narrowed retinal arterioles
What is psuedotumour cerebri
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
What is optic neuritis
Diverse group for inflammatory optic nerve diseases caused by demyelination of optic nerve neurons leading to axonal injury and apoptosis
Etiologies of optic neuritis
Atypical or Typical
Atypical optic neuritis
From infection of autoimmune
Typical optic neuritis
Usually idiopathic or a demyelinating lesion like MS
What is the optic neuropathy triad
Vision loss, periocular pain and dychromatopsia
Three types of otpic nerve damage
Retrobulbar neuritis, Papillitis, Neuroetinitis
What is retrobulbar neuritis
2/3 Optic nerve cases where ONH appears normal but thats due to the inflammation is posterior to the globe
What is papillitis
Inflammation of the ONH, ONH hyperaemia, oedema and peripapillary flame haems
What is neurotinitis
Papilliis with inflammation of the RNFL and a Macular star
What is MS
chronic demyelinating and neurodegenerative disease of the CNS where scarring forms in response to demyelination leading to neurological dysfunction and disability over time
Who is affected by MS and the consequence of MS
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
What does AION stand for
Anterior ischaemic optic neuropathy
What is anterior ischemic optic neuropathy
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
Two classifications of AION - Anterior ischemic optic neuropathy
Arteritic AION and Non-arteritic AION
What is Arteritic AION
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.
Arteritic AION symptoms
Temporal headache, Jaw Claudification, fevers, proximal muscle pain and stiffness. Diplopia also seen
WHat is Non-Arteritic AION
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.
Non-arteritic AION systemic associations
Hyperlipidemia and atherosclerotic diseases like angina and stroke
Non-arteritic AION ocular associations
Disc and risk in the fellow eye
What is Age related Macular Degeneration ( AMD )
Common irreversible blindness associated with Macular Drusen at the bruchs membrane
Who does AMD effect
Older caucasions over 65
AMD progression and where does it affect
Slow and affects central vision
How to detect AMD
using Amsler grid
What does macular drusen look like
Like the surface of the sun around the macular
AMD risk factors
Age, lighter iris colour, smoking, UV and higher BMI
How does smoking cause AMD
Increases AMD severity and lowers antioxidants
What can reduce AMD
Red wine, green vegetables and vitamin supplements
Why does AMD have central vision loss
High density of photoreeptors needing high oxygen demand, not enough oxygen
What is the only blood supply to the central retina
The choroid
What happens to blood supply in the retina with age and its effects
Decreases choriocapillaris density and lumen diameter which decreases blood flow so oxidative damage increased to ocular tissue
Where is Macular drusen found
Between bruchs membrane and the RPE
Where is the RPE
Single layer between Bruchs membrane and photoreceptors
Function of the RPE
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
When are rods and cones phagocytosed
Rods in the morning and Cones in the evening
Causes of AMD
Lipofuscin deposits, Oxidative stress, reduced choroidal blood flow and chronic inflammation
How does lipofuscin cause AMD
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
How do changes in the choroid cause AMD
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
How does Chronic inflammation cause AMD
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
Two types of AMD
Atrophic ( Dry ) and Exudative ( Wet )
What is atrophic AMD
90% cases, has drusen progressing into Grographic atrophy of the macular and reduced vision
What is exudative AMD
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
Treatment for atrophic AMD
Monthly intravitreal injections of pegcetacoplan which slows geographic atrophy but increased chances of conjunctival hemorrhage with increased IOP and blurred vision
Treatment for Exudative AMD
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
Current statistics and characteristics for myopia
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
What does myopia depend on
Genetics and Environment
Consequence of eye elongation in myopia
This is a scleral abnormality. Here the retina and the choroid are stretched and becomes thinner and damaged resulting in myopic maculopathy
Classification of myopia
Mild myopia –> Less than -3.00D
Moderate Myopia –> -3.00D - -6.00D
High myopia –> more than -6.00D
Other health risks in having myopia
Increased risk of glaucoma and cataracts. It is also associated with an increased risk of pathology
What does increasing myopia mean for the patient
Increased risk for Myopic Maculopathy and retinal detachment
Explain the onset of Myopia
Occurs in childhood and progresses and stabilises around the 20 years of age
Describe the fundus changes seen in Myopia
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
What is observed in optic disc crescent
Usually on the temporal side of disc
What is observed in Tessellated Fundus
Choroidal vessels visible due to hypoplasia of RPE cells
What is observed in staphyloma and chorioretinal atrophy
Bulging of the temporal walls in the orbit in an MRI scan
Arcuate vasculature becomes straightened
What is observed in Lacquer cracks in Myopia
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
What is observed in Fuch’s spot
Occurs with Foveal Choroidal Neovascularisation and haemorrhage that leaves scars and a central scotoma in their vision
What is Macular Retinoschesis in high myopia
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
Describe the 4 Treatments for slowing myopia progression and how they work
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
Describe Central Serous Retinopathy and its characteristics
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
What is a type A personality
Job involvement, competitiveness and impatience
What is a Cystoid Macular Edema ( CME / CMO )`
Fluid-filled microcysts in the retina which can coalesce into larger cysts
These cysts can break through to form macular holes
Cystoid Macular Edema Etiologies
Diabetic neuropathy, Uveitis, Idiopathic and Retinitis Pigmentosa
Causes of Macular holes
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
What does an Epiretinal membrane look like
From fine, glistening membrane overlying the macula to thick and white tissue obscuring the retinal bvs which may cause traction and retinal pucker
Characteristics of Epiretinal membranes
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
Name the two Toxic Maculopathies
Chloroquine and Tamoxifen Maculopathy
Chloroquine maculopathy
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
Tamoxifen Maculopathy
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
What is Thiazolidinediones ( TZDs )
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
What is the side effect of Thiazolidinediones
Macula Edema
