Optho part five Flashcards
Aqueous humor
a. Production
i. Ciliary body
b. Circulation
i. movement from posterior to anterior chamber
Outflow pathway
i. Trabecular meshwork – fine meshwork that filters the aqueous fluid from the eyes.
ii. Uveoscleral outflow tract – venous outflow from the uveoscleral tract also facilitates the removal of aqueous from the eye.
Optic nerve
Glaucoma may be defined as an optic neuropathy, believed to be caused by an intraocular pressure that the optic nerve can not tolerate.
Injury to axons from retinal ganglion cells at lamina cribrosa
. Increased size of central cup
Asymmetric cupping – higher risk than symmetrical cupping.
Open angle glaucoma
a. Increased intraocular pressure
b. African and Caribbean ancestry
c. Age greater than 75 years
d. Primary family member with glaucoma
e. Lack of symptoms until late in disease
Angle closure glaucoma: Risk factors
i. Anatomically narrow anterior chamber angle
ii. Hyperopia
iii. Pharmacologic dilation of pupil
iv. Older age
vi. Some Asian populations
Angle closure glaucoma: SX
i. ocular pain
ii. ocular redness
iii. Blurred vision, halos, nausea
Angle closure glaucoma: Signs
i. Dilated fixed pupil (classically mid-dilated)
ii. Narrow anterior chamber angle
iii. pupillary block
iv. Corneal edema
Pharmacologic treatment for open angle glaucoma: Medications that increase aqueous humor outflow
a. Parasympathomimetics – reduce the intraocular pressure by increasing aqueous outflow. It is believed that the effect of the pupillary constriction on the ciliary muscle opens up the trabecular meshwork and facilitates aqueous outflow.
b. Prostaglandin analogues – increase outflow via the uveoscleral tract, can cause ocular redness and increased lash growth. Systemic side effects are the same as oral beta-blockers.
Pharmacologic treatment for open angle glaucoma: Medications that decrease aqueous production
a. Topical beta blockers – reduce the intraocular pressure by decreasing aqueous secretion by the ciliary body. The exact pharmacological basis is unclear.
b. Carbonic anhydrase inhibitors – reduce aqueous secretion through direct inhibition of the enzyme carbonic anhydrase.
i. Topical – less effective, less side effects
ii. Oral – more effective, more side effects.
c. Alpha-2-agonists – lower IOP by decreasing aqueous production and enhancing uveoscleral outflow.
d. Adrenergic agonists – increases aqueous outflow through beta agonist action. Uncommon currently, can lead to black deposits in the eye
Pharmacologic treatment for open angle glaucoma: Surgical treatment: Acute angle closure glaucoma
a. Peripheral iridectomy – allow alternative route for aqueous to pass from the anterior chamber.
b. Laser peripheral iridotomy – more common practice currently.
Pharmacologic treatment for open angle glaucoma: Surgical treatment: Open angle glaucoma
a. Laser trabeculoplasty – temporarily increases out flow by enlarging the openings in the mesh work
b. Filtering surgery – alternative outflow
c. Tube implantation – alternative outflow when filter is likely to fail.
d. cyclodestruction - decrease production by decreasing amount of functioning ciliary body tissue.
medial rectus
innervated by CN III, origin at the annulus of Zinn in the posterior part of the orbit and inserts 5.5 mm from the limbus on the medial side of the globe. Its sole action is adduction.
lateral rectus
innervated by CN VI, origin at the annulus of Zinn and inserts 6.9mm from the limbus on the lateral side of the globe. Its sole action is abduction.
superior rectus –
innervated by CN III, originates from the upper part of the annulus of Zinn and inserts 7.7mm from the superior limbus. Its primary action is elevation, its secondary actions are adduction and intortion.
Inferior rectus
– innervated by CN III, originates at the lower part of the annulus of Zinn and inserts 6.5 mm from the inferior limbus. Its primary action is depression, its secondary actions are abduction and extorsion.
superior oblique
innervated by CN IV, originates above and medial to the optic foramen. It passes through the trochlea at the angle between the superior and medial orbital walls and is reflected backwards to insert in the posterior upper temporal quadrant of the globe. Its primary action is intorsion, its secondary actions are depression and abduction.
inferior oblique
innervated by CN III, originates from a small depression just behind the orbital rim and lateral to the tear duct. It passes backwards to insert on the inferior posterior quadrant of the globe close to the macula. Its primary action is extorsion and secondary actions are elevation and abduction.
Levator palpebrae superioris muscle
innervated by CN III, originates on the lesser wing of the sphenoid bone, just above the optic foramen. It broadens and becomes the levator aponeurosis. This portion inserts on the skin of the upper eyelid, as well as the superior tarsal plate. Its action is the elevation of the eyelid.
Arterial
All extraocular muscles are supplied by the lateral and medial muscular branches of the ophthalmic artery. The lateral branch supplies the lateral and superior rectus muscles, the levator muscle of the upper lid, and the superior oblique muscle. The medial branch, the larger of the two, supplies the inferior and medial rectus muscles and the inferior oblique muscle. The inferior rectus muscle and the inferior oblique muscle also receive a branch from the infraorbital artery, and the medial rectus muscle receives a branch from the lacrimal artery.
Venous
The veins from the extraocular muscles correspond to the arteries and empty into the superior and inferior orbital veins, respectively.
Amblyopia
potentially permanent loss of vision due to asymmetric visual input or from vision deprivation.
Strabismic amblyopia (major cause of unilateral decreased vision in children)
monocular suppression of the deviating eye.
Refractive amblyopia (anisometropic)
– caused by a difference in refractive error (as little as 1 diopter). Superimposition of a focused and unfocused image leads to suppression of the blurred image.
Form deprivation and occlusion amblyopia
a deprivation of visual stimuli, often due to a congenital cataract, eye lid mass or ptosis.
