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