Ocular system Flashcards

1
Q

Describe the anatomy of the eye?

A

The sclera is the thick, white connective tissue capsule around the eye and the cornea is a specialised region which is clear and dense.

The choroid is specialised into the iris, ciliary muscle and suspensory ligaments…

The action of the ciliary muscle and tension they enact on the suspensory ligaments determines the shape + therefore focusing power of the lens.

The retina contains photoreceptors, rods + cones.

Overall, eye is divided into 2 fluid-filled spaces for support.
At the front, between iris and cornea is the aqueous humour.

Between the lens and retina = viscous, vitreous humour.

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2
Q

What smooth muscle is there in the eye?

A

To regulate PUPIL = In the iris, there are two layers of SM.
Dilator (radial) and Sphincter (constrictor) SM = which regulates size of the pupil and therefore amount of light reaching the retina.
= Innervated by autonomic nerves

To regulate LENS = Ciliary SM tension applies to suspensory ligaments, to control the shape for accomodation of the lens.

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3
Q

What is the process of pupil dilation?
How does parasympathetic NS affect the lens?

A

Mydriasis = pupil dilation from radial (dilator) SM contraction.
= Sympathetic NS.
= NA acts on a1 adrenoceptors.

Sympathetic fibres from superior cervical ganglion.

Sympathetic NS = mydriasis = pupil dilation.
BUT
no effect on lens as ciliary muscle has no adrenergic receptors.
A1 agonism on radial SM causes pupillary dilation.

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4
Q

What is the process of pupil constriction?

A

Miosis =pupil constriction by contraction of Sphincter (constrictor) SM.

= ACh released acts on M3 muscarinic receptors.
= Parasympathetic NS.

= Cranial parasympathetic axons innervate the ciliary ganglion, from which postganglionic parasympathetic fibres innervate the sphincter SM.

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5
Q

How is Iris tone usually maintained?
What are consequences of overactivity?

A

Parasympathetic signalling is dominant over Sympathetic signalling.
= Inducing Sphincteric SM contraction - causing pupil dilation via ACh at M3 receptors.

= Miosis = pinpoint pupils.
= Mydriasis = dilated pupils.

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6
Q

How do a1 receptors and M3 receptors carry out SM contraction?

A

a1 receptors and M3 receptors are both Gq coupled…
= PIP2 -> IP3 + DAG
= Ca2+ release.
= Ca2+/Calmodulin binds MLCK.
= MLCK uses ATP to phosphorylate myosin cross-bridges.
= Which can bind to actin = SM contraction.

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7
Q

What is the pupillary light reflex?

Vs Pupillary dark response?

A

In bright light = miosis.
In low light = mydriasis.

Consensual response = response in one eye should stimulate the other eye = Important for diagnostics.

In order to protect photoreceptors from bright lights…

Pupils usually dilate when its dark - relaxation of iris sphincter (constrictor) and contraction of iris radial/dilator SM

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8
Q

What is Angel’s trumpet?

A

A flow which contained scopolamine, hysocyamine, and atropine….
Causes the eye it touches to lose pupillary light reflex and accomodation.

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9
Q

What happens to the pupils and lens when muscarinic agonists/antagonists are applied?

A

Muscarinic agonist = M3 receptor activation = Contraction of sphincter pupillae.
= Miosis = pupils constrict.

M3 activation causes ciliary muscle contraction = lens contracts = Near sight.

Muscarinic antagonist = block contraction of sphincter pupillae = mydriasis = pupils dilate.

Ciliary muscle relaxation = lens relaxes = far sightedness

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10
Q

What are the class names of muscarinic antagonists?

A

Mydriatics = block constrictor/sphincter muscle = pupillary dilation.

Cycloplegics = paralyse ciliary muscle to block accomodation.

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11
Q

What are the uses of muscarinic antagonists?

A

Tropicamide = short-lasting anti-muscarinic used during ocular examination, to cause mydriasis for better visualisation of the retina…

Lazy eye/amblyopia = Use atropine on the good eye, to blur vision in good eye + force use of slow eye.

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12
Q

What is glaucoma?
What diseases can cause glaucoma?
What are the symptoms of glaucoma?

A

Optic nerve damaged, tends to be due to increased intraocular pressure : depending on volume of aqueous humour.

Diabetes, hypertension, age.

Intra-ocular pressure above 21mmHg, optic nerve damage and loss of peripheral vision.

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13
Q

What is the role of the aqueous humour?

A

The aqueous humour is produced by ciliary body epithelium to provide nutrients to cornea, lens, etc. and maintain intraocular pressure.

The cornea and lens are avascular!!

(AH is anterior/in front of lens and iris, between the cornea).

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14
Q

How does aqueous humour circulate?

A

AH produced by the ciliary body, flowing from posterior chamber through the iris into the anterior chamber in front of iris…

AH drains through (90%) trabecular meshwork, through Canal of Schlemm into veins…. with some via uveoscleral outflow.

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15
Q

What is open-angle glaucoma?

A

There is obstruction/blockage of drainage through Trabecular meshwork and Canal of Schlemm, reducing AH drainage into veins.

So the drainage of anterior chamber is reduced and intraocular pressure rises, causing optic nerve damage.

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16
Q

How is aqueous humour formed?

What stimulate AH formation?

A

Aqueous humour is produced continuously by ultrafiltration of blood plasma in the ciliary body.

Through an active secretion process.

=Increased by beta-agonists, decreased by alpha agonists…

Therapeutically = beta-antagonists, alpha agonists.

Vasodilation with beta-agonists = increased AH formation.

Vasoconstriction with a1 agonists = decrease AH formation.

a2 agonists = present on pre-synaptic neurone = autoreceptor = reduce the sympathetic release of NA AND present on ciliary body = reduce cAMP = also directly reduce AH formation.

17
Q

What alpha agonists are used to treat glaucoma?

Unwanted effects?

A

Dipivefrin = prodrug of epinephrine/Adrenaline as eye drops.
Stimulates both alpha and beta receptors!

Brimonidine = a2 agonist = most common!
Directly inhibits AH formation by decreasing cAMP as well as presynaptic inhibition reducing NA release…
Side-effects = fatigue + drowsiness?

18
Q

What beta-adrenoceptor antagonists are used for glaucoma?

A

Beta adrenoceptors are used topically!!!
Beta adrenoceptors stimulate AH formation.
= need to antagonise to reduce AH formation.

Timolol is the most common = non-selective beta blocker
But is not B1 selective.

19
Q

How is carbonic anhydrase involved in glaucoma?

A

AH formation requires active transport of HCO3- ions from ciliary body, into AH.

Generating HCO3- requires CA.

CA inhibitors can be used to reduce AH formation.

20
Q

What is the MOA of brinzolamide?

A

Brinzolamide = topical carbonic anhydrase inhibitor used to treat glaucoma.
AH formation requires active transport of HCO3- ions into AH, therefore, CA anhydrase inhibition reduces AH formation.
= long-half life, frequently used.

21
Q

How can normal and raised glaucoma treated by improving drainage of AH?

A

To improve drainage through trabecular meshwork then through Canal of Schlemm:

Muscarinic agonists like Carbachol and Pilocarpine!
(BUT ALSO ACT AS MIOTICS = pupil constrictors)…
contraction of ciliary muscle puts tension on trabechular meshwork - opening pores + facilitating AH outflow.

Improved drainage through uveoscleral flow:
Prostaglandin analogues like Latanoprost PGF2a analogue.

22
Q

What combination therapies are there for glaucoma?

A

Typically, involve using timolol = non-selective beta blocker to reduce stimulation of AH formation.

Alongside brinzolamide = CA inhibitor = reduce AH formation
Alongside Brimonidine = alpha agonist = reduce AH formation
Alongside PGF2a analogues = prostaglandins

23
Q

What is closed-angle glaucoma?

A

Where the angle of iris and cornea is narrowed and AH flow from posterior to anterior chamber is blocked!
EMERGENCY, with sudden onset and cause irreversible damage!

24
Q

How is closed-angle glaucoma treated?

A

Increase blood osmolarity and cause water loss of vitreous humour, reduce intraocular pressure…

Mannitol = most common = diuretic.
Or laser surgery = burn holes in trabecular meshwork or remove portion of iris.

25
Q

How does allergy affect the eyes?

A

Cause itchiness and reddening.
= due to IgE-mediated mast cell degranulation.

Use H1 antagonists, Cromones to stabilise mast cells, glucocorticoids but run risk of developing glaucoma or cataracts.

26
Q

What is dry eyes?

A

Reduced secretion.
After radiotherapy, Sjogren’s syndrome or keratoconjunctivitis.

Treated with pilocarpine = muscarinic agonist = more tears.
Glucocorticoids/immunosuppressants = Sjogrens syndrome.
Lifitegrast = A1, B2 antagonist,

27
Q

What is “Wet AMD”?

A

Choroidal neovascularisation = excessive blood vessel growth under retina.

Treated with photodynamic therapy = verteporfin followed by laser activation… to occlude leaky blood vessels.

But causes scarring…

or reduce blood vessel growth with anti-VEGF antibodies/binding molecules like pegaptanib.

28
Q

What is macular degeneration?

A

Macula is part of retina essential for sharp vision, with most concentration of cones.
AMD is age-related macular degeneration.
Dry AMD = atrophy of the macula. Slow onset without treatment :(