Optho part five

Question 1

Aqueous humor

Answer 1

a. Production
i. Ciliary body
b. Circulation
i. movement from posterior to anterior chamber

Question 2

Outflow pathway

Answer 2

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.

Question 3

Optic nerve

Answer 3

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.

Question 4

Open angle glaucoma

Answer 4

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

Question 5

Angle closure glaucoma: Risk factors

Answer 5

i. Anatomically narrow anterior chamber angle
ii. Hyperopia
iii. Pharmacologic dilation of pupil
iv. Older age
vi. Some Asian populations

Question 6

Angle closure glaucoma: SX

Answer 6

i. ocular pain
ii. ocular redness
iii. Blurred vision, halos, nausea

Question 7

Angle closure glaucoma: Signs

Answer 7

i. Dilated fixed pupil (classically mid-dilated)
ii. Narrow anterior chamber angle
iii. pupillary block
iv. Corneal edema

Question 8

Pharmacologic treatment for open angle glaucoma: Medications that increase aqueous humor outflow

Answer 8

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.

Question 9

Pharmacologic treatment for open angle glaucoma: Medications that decrease aqueous production

Answer 9

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

Question 10

Pharmacologic treatment for open angle glaucoma: Surgical treatment: Acute angle closure glaucoma

Answer 10

a. Peripheral iridectomy – allow alternative route for aqueous to pass from the anterior chamber.
b. Laser peripheral iridotomy – more common practice currently.

Question 11

Pharmacologic treatment for open angle glaucoma: Surgical treatment: Open angle glaucoma

Answer 11

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.

Question 12

medial rectus

Answer 12

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.

Question 13

lateral rectus

Answer 13

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.

Question 14

superior rectus –

Answer 14

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.

Question 15

Inferior rectus

Answer 15

– 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.

Question 16

superior oblique

Answer 16

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.

Question 17

inferior oblique

Answer 17

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.

Question 18

Levator palpebrae superioris muscle

Answer 18

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.

Question 19

Arterial

Answer 19

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.

Question 20

Venous

Answer 20

The veins from the extraocular muscles correspond to the arteries and empty into the superior and inferior orbital veins, respectively.

Question 21

Amblyopia

Answer 21

potentially permanent loss of vision due to asymmetric visual input or from vision deprivation.

Question 22

Strabismic amblyopia (major cause of unilateral decreased vision in children)

Answer 22

monocular suppression of the deviating eye.

Question 23

Refractive amblyopia (anisometropic)

Answer 23

– 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.

Question 24

Form deprivation and occlusion amblyopia

Answer 24

a deprivation of visual stimuli, often due to a congenital cataract, eye lid mass or ptosis.

Question 25

Strabismus: 1. Concomitant vs. incomitant

Answer 25

1. Concomitant vs. incomitant - strabismus can be concomitant, where the size of the deviation does not vary with direction of gaze—or incomitant, where the direction of gaze does affect the size, or indeed presence, of the ocular misalignment. The majority of deviations are concomitant and begin early in childhood, typically between the ages of 2 to 4 years. Incomitant deviations occur both in childhood and adulthood as a result of neurological, mechanical or myogenic problems affecting the muscles controlling eye movements.
2. Tropia vs. Phoria

Question 26

Types of misalignment

Answer 26

a. Esotropia – eyes pointing in (crossed eyes)
b. Exotropia – eyes pointing out (wall eyed)
c. Hypertropia – an eye pointed upward
d. Hypotropia – an eye pointing downward

Question 27

Leukocoria

Answer 27

1. Retinoblastoma
2. Retinopathy of prematurity
3. Cataract

Question 28

Leukocoria: Retinopathy of prematurity

Answer 28

• Second most common cause of childhood blindness next to cortical blindness in United States
  Blood supply to eye initially provided by the hyaloid artery originating from optic nerve, passing through vitreous supplying vessels to lens and iris
  These vessels USUALLY are resorbed by 34 weeks gestation
  Blood vessels appear in retina at 15-18 weeks gestation, extending out from optic disk peripherally
  Nasal vascularization completed first, temporal last

Question 29

Leukocoria: Retinopathy of prematurity: Pathogenesis

Answer 29

of ROP is not well understood
Initial injury
Hypoxia, hypotension, hyperoxia, free radical formation > injury of newly formed blood vessels
Resumption of normal growth OR neovascularization with ↑ permeability > retinal edema and hemorrhage > abnormal fibrovascular tissue > contract and put traction on the retina > retinal distortion or detachment
? Role of vascular endothelial growth factor (VEGF), IGF-1

Infants > 32 weeks are not at risk for developing ROP
Most infants born >28 weeks who develop ROP have mild disease not requiring treatment
Treatment of choice is ablation of the peripheral avascular retina via photocoagulation using a diode or argon laser which has reduced bad structural and functional outcomes

Question 30

Leukocoria: Cataract

Answer 30

congenital opacity of the lens, often associated with intrauterine infection.