The Eye Flashcards
What is neurotrophic keratitis?
Caused by damage to trigeminal nerve which results in damage in tear ducts, therefore decrease vitamins and Gf into the cornea causing corneal epithelial breakdown and ulceration
How is aqueous humor produced?
Active secretion and ultrafiltration by ciliary epithelium (part of ciliary bodies) which suspend lens
What happens during posterior vitreous detachment
Not harmful in itself until it pulls the retina, but it causes floaters in vision
What are the visual photoreceptor cells of the retina?
Cones- used in brighter light to see colour
Rods - extremely sensitive, used at low light levels and do not mediate colour vision (located further away from fovea)
What is the Walds visual cycle?
In the dark, cGMP levels are high and keep cGMP-gated sodium channels open allowing a steady inward current, called the dark current. This dark current keeps the cell depolarised at about -40 mV, leading to glutamate release which inhibits excitation of neurons
Light closes cGMP-gated sodium channels, reducing the influx of both Na+ and Ca2+ ions. Stopping the influx of Na+ ions effectively switches off the dark current. Reducing this dark current causes the photoreceptor to hyperpolarise, which reduces glutamate release which thus reduces the inhibition of retinal nerves, leading to excitation of these nerves. This reduced Ca2+ influx during phototransduction enables deactivation and recovery from phototransduction
What is RPE?
Retinal pigment epithelium (RPE) is the pigmented cell layer just outside the neuro-sensory retina that nourishes retinal visual cells and had multiple functions: here are a few:
- lAbsorption of scattered light to improve the quality of the optical system
- epithelial transport: RPE supply nutrients to photoreceptors, control ion homeostasis and eliminate water and metabolites
- Phagocytosis of photoreceptor outer segment (POS) membranes: POS are exposed to constant photo-oxidative stress, and they go through constant destruction by it. They are constantly renew, by shedding the ends and then RPE phagocytose and digest these segments.
What is the optic nerve?
The optic nerve, also known as CN II, is a paired nerve that transmits visual information from the retina to the brain
The optic nerve transmits all visual information including brightness perception, colour perception and contrast (visual acuity).
The eye’s blind spot is a result of the absence of photoreceptors in the area of the retina where the optic nerve leaves the eye.
What are 3 examples of optic nerve damage?
- Glaucoma (Transport problem)
- Leber hereditary optic neuropathy (mitochondrial DNA)
- dominant optic atrophy (Genetic disorder)
What is Glaucoma?
major risk factors
Key findings on examination?
Glaucoma is a group of eye diseases which result in damage to the optic nerve and vision loss.
- The most common type open-angle glaucoma develops slowly over time and there is no pain. Peripheral vision may begin to decrease followed by central vision resulting in blindness if not treated.
- closed-angle glaucoma can present gradually or suddenly. The sudden presentation may involve severe eye pain, blurred vision, mid-dilated pupil, redness of the eye, and nausea. Vision loss from glaucoma, once it has occurred, is permanent.
The major risk factor for most glaucomas and the focus of treatment is increased intra-ocular pressure, problems with axoplasmic flow. Intra-ocular pressure is a function of production of liquid aqueous humour by the ciliary processes of the eye, and its drainage through the trabecular meshwork.
Key finding:
Cotton wool spots are an abnormal finding on funduscopic exam of the retina of the eye. They appear as fluffy white patches on the retina. They are caused by damage to nerve fibers and are a result of accumulations of axoplasmic material within the nerve fiber layer.
Describe the mitochondrial placement of the optic nerve head
Cytochrome C stain for mitochondria indicates the mt is located at the top before it passes through the lamina cribrosa - The nerve fibers forming the optic nerve exit the eye posteriorly through a hole in the sclera that is occupied by a mesh-like structure called the lamina cribrosa where myelination is prevalent on optic nerve after the lamina cribrosa
2 possible explanations for mt placement:
1. axonal constriction by lamina beams
2 mitochondria ‘held’ in place according to physiological need as lots of Na+ channels present without myelination
What is Leber’s hereditary optic neuropathy (LHON)?
Who does it affect more?
How do patients present?
is a mitochondrially inherited (transmitted from mother to offspring) degeneration of retinal ganglion cells (RGCs) and their axons that leads to an acute or subacute loss of central vision
Affects Male> female by 5x
Presentation: caecocentral scotoma, acute disc swelling and pupils usually spared in early vision but it is a central vision problem
What is the clinical presentation of LHON?
Clinically, there is an acute onset of visual loss, first in one eye, and then a few weeks to months later in the other. Onset is usually young adulthood, but age range at onset from 7-75 is reported.
This typically evolves to very severe optic atrophy and a permanent decrease of visual acuity.
Examination reveals decreased visual acuity, loss of color vision and a cecocentral scotoma, vascular tortuosity, telangiectatic vessels around optic disc, swelling of the retinal nerve fibre layer on visual field examination.
Describe the genetics of LHON
- It is a primary mitochondrial DNA disorder
- Three mtDNA point mutations account for ~90% of cases
- 11778G>A is the most common mutation, others are 14484T>C and 3460G>A
- primary LHON mutations tend to be specific to retinal ganglion cells (RGC)
How are RGC affected in LHON?
What causes its destruction?
RGC are preferentially affected in LHON
Experimental evidence reveals impaired glutamate transport and increased reactive oxygen species (ROS) causing apoptosis of retinal ganglion cells.
Describe the mitochondrial respiratory chain
Mitochondrial DNA makes 13 proteins where 4 out of 5 complexes have subunits are encoded by mitochondrial genome.
The electron transport chain: transfer electrons from electron donors to electron acceptors via redox (both reduction and oxidation occurring simultaneously) reactions, and couples this electron transfer with the transfer of protons (H+ ions) across a membrane. This creates an electrochemical proton gradient that drives the synthesis of adenosine triphosphate (ATP)