Orbit/Glaucoma (Week 1--Melega) Flashcards
What goes through the optic canal?
Optic Nerve (CN II)
Ophthalmic artery
What goes through the superior orbital fissure?
Occulomotor nerve (CN III)
Trochlear nerve (CN IV)
Ophthalmic nerve (CN V1)
Abducent nerve (CN VI)
Superior ophthalmic vein
Inferior ophthalmic vein (one part)
What goes through the inferior orbital fissure?
Maxillary nerve branches (CN V2)
Maxillary artery branches
Inferior ophthalmic vein (one part)
Walls of orbit shared with paranasal sinuses
Orbital plate of frontal bone with frontal sinus
Thin plate of ethmoid bone with ethmoid sinus
Orbital plate of maxillary bone with maxillary sinus (infraorbital nerve in wall)
Fascial sheath
Forms socket for eyeball
Pierced by tendons of extraocular muscles
Forms check ligaments (medial check ligament, lateral check ligament, suspensory ligament) that make sure you can’t turn your eyeballs too far in one direction
Orbital fat provides cushion
Periosteum is called periorbita (lines bone of the orbit)
7 extraocular muscles
1) Levator palpebrae superioris (CN III superior): elevate upper eyelid
2) Superior oblique muscle (CN IV): rotate in/intortion
3) Inferior oblique muscle (CN III inferior): rotate out/extortion
4) Superior rectus muscle (CN III superior): look up/elevation
5) Inferior rectus muscle (CN III inferior): look down/depression
6) Medial rectus muscle (CN III inferior): look in/adduction
7) Lateral rectus muscle (CN VI): look out/abduction
3 somatic motor nerves
1) Occulomotor nerve (CN III)
2) Trochlear nerve (CN IV)
3) Abducent nerve (CN VI)
Occulomotor nerve (CN III)
Superior division: innervates levator palpebrae superioris muscle, superior rectus muscle
Inferior division: innervates medial rectus muscle, inferior rectus muscle, inferior oblique muscle
Trochlear nerve (CN IV)
Innervates superior oblique muscle
Abducent nerve (CN VI)
Innervates lateral rectus muscle
3 coats of wall of eyeball
Fibrous coat
Uvea
Retina
Fibrous coat
Cornea: anterior 1/6; avascular; somatic sensory (CN V1)
Sclera: posterior 5/6; pierced by optic nerve and ophthalmic vessels; attachment point for extraocular muscles
Limbus: corneoscleral junction
Uvea
Vascular pigmented coat
Choroid: highly vascular
Ciliary body: ciliary muscle (smooth muscle, parasympathetic), ciliary processes become zonules that attach to lens, capillaries (vitreous humor production)
Iris: sphincter pupillae muscle (smooth muscle, paraympathetic, circular muscle?), dilator pupillae muscle (smooth muscle, sympathetic)
Pupil
Retina
Retinal pigment epithelium
Neurosensory retina
Optic disc forms optic nerve that penetrates lamina cribrosa of sclera; central retinal artery/vein also passes through
Optic chiasm
Eyeball interior
Lens (elastic qualities)
Vitreous chamber with vitreous body (proteoglycans/hyaluronan)
Aqueous humor fills anterior part, which has 2 chambers (posterior chamber and anterior chamber)
What happens to the vitreous chamber at 40 - 70 years of age?
Vitreous becomes more liquid and can detach from retina (vitreous detachment) which causes flaskes of light/floaters
If fluid gets into retina get retinal detachment (serious visual problem)
What is the flow of aqueous humor?
Aqueous humor produced by epithelium lining ciliary process of ciliary body –> into posterior chamber –> through pupil –> into anterior chamber –> into trabecular meshwork –> into canal of Schlemm –> scleral veins
What is aqueous humor?
Produced by epithelium lining ciliary processes of ciliary body
Protein-free ultrafiltrate of blood plasma
Maintains shape of anterior eyeball
Nourishes cornea and lens
Ophthalmic nerve (CN V1)
Lacrimal nerve to lacrimal gland
Frontal nerve to upper eyelid and forehead (supraorbital nerve and supratrochlear nerve)
Nasociliary nerve (ciliary ganglion branches pass through ciliary ganglion and become short ciliary branches for sensory to iris and cornea; long ciliary branches are to iris and cornea; ethmoid branches to nasal cavity; infratrochlear branches to medial eyelid)
Ciliary ganglion roots
Parasymp pre fibers from oculomotor nerve (CN III) symapse in ganglion
Somatic sensory fibers from ophthalmic nerve (CN V1) pass through
Sympathetic fibers from surface of internal carotid artery (superior cervical ganglion) pass through
Short ciliary nerves
Branches off ciliary ganglion
Parasymp post fibers to ciliary muscle and to sphincter pupillae muscle
Somatic sensory fibers from ophthalmic nerve (CN V1) FROM cornea and iris
Sympathetic fibers to blood vessels in choroid
Sympathetic fibers of the orbit
Symp pre cell bodies in T1 - 4 –> symp post cell bodies in superior cervical ganglion –> symp post fibers course on surface of internal carotid artery
2 courses of sympathetic fibers
Ciliary ganglion (no synapse) –> short ciliary nerves –> blood vessels in choroid
Long ciliary nerves (branches of ophthalmic nerve-nasociliary) –> dilator pupillae muscle in iris
Ophthalmic artery
Central artery of retina
Ciliary arteries supply choroid
Lacrimal artery
Supraorbital and supratrochlear arteries
Anterior and posterior ethmoid arteries
Muscular branches
Ophthalmic veins
Superior ophthalmic vein –> superior orbital fissure –> cavernous sinus
Inferior ophthalmic vein branch –> superior orbital fissure –> cavernous sinus
Inferior ophthalmic vein branch –> inferior orbital fissure –> pterygoid venous plexus
Optic disc
Small white area where there are no photoreceptors
Optic nerve (CN II) passes through
Entrance of ventral artery of retina (branches don’t anastomose with each other = end artery)
Exit of central vein of retina
Sympathetic innervation of the eye
NE –> alpha 1 receptors –> contract radial smooth muscle of iris (dilator pupillae) –> mydriasis (bigger pupil)
Parasympathetic innervation of the eye
1) ACh –> muscarinic receptor –> contract sphincter smooth muscle of iris (constrictor pupillae) –> miosis (smaller pupil)
2) ACh –> muscarinic receptor –> contract ciliary body –> accommodation
Accommodation
Light from single point of distant object and light from single point of near object being brought to a focus by changing curvature of the lens
Ciliary body muscle contracts and moves anteriorly –> relaxes tension on suspensory ligaments that support lens –> lens becomes more convex (rounds up in shape) –> eye focuses on nearby object
Accommodation development and age-dependence
Effective by age 4 months
Remains adequate until onset of presbyopia at 40 years old
Presbyopia
Condition in which lens of eye loses some ability to focus which makes it difficult to see objects up close
Also continuing appositional growth of lens fibers and age-related changes in lens capsule causes elasticity of lens to diminsh ??
Cycloplegia
Paralysis of ciliary muscle of eye
results in loss of accommodation
Due to devervation or pharmacologic action (ACh antagonist like atropine)
Relationship between mydriasis and accommodation
Mydriasis can occur without loss of accommodation (alpha 1 agonist)
If have loss of accommodation, then will have mydriasis (muscarinic antagonist)
Alpha 1 only at pupillary dilator smooth muscle
ACh at both ciliary muscle and pupillary sphincter smooth muscle
Mydriatic agents (increase pupil size)
Sympathomimetics (alpha 1 agonists): phenylephrine
Parasympatholytics (muscarinic antagonists): atropine
Miotic agents (decrease pupil size)
Parasympathomimetics (cholinergic agonists)
Sympatholytics (alpha 1 antagonists)
Opioids
How do opioids cause miosis?
Opioid inhibitory interneurons maintain inhibitory tone on Edinger-Westphal cell bodies (para pre that regulate para contraction of pupillary sphincter smooth muscle of iris) –> opiods bind receptors on these interneurons and cause them to have less inhibition of E-W pre neurons so they fire more rapidly and lead to more activation of para post neurons –> contraction of pupillary sphincter smooth muscle of the iris –> miosis
Aqueous humor production and outflow
Produced by ciliary body and derived from plasma capillary network
Secretion of Na+ and HCO3- into aqueous humor draws water in osmotically
Drained mostly through trabecular meshwork to Canal of Schlemm; also via uveoscleral pathway (<10% of total)
Glaucoma
Group of diseases that can damage optic nerve and cause vision loss/blindness
Obstruction of aqueous drainage –> elevated intraocular pressure –> damage to optic nerve (more than 1 million fibers connecting retina to brain)
Open-angle glaucoma
Angle between peripheral iris and cornea is normal
Drainage of aqueous humor affected due to clogging of trabecular meshwork
Increased IOP, degeneration of optic head, restricted visual field all typify primary open-angle glaucoma
Symptoms: generally field of vision narrowed so cannot see clearly
Closed-angle glaucoma
Angle between iris and cornea narrows which blocks drainage of aqueous humor
Rarer, but severe, acute form of disease can cause blindness if not treated in 24 - 48 hours
Sudden increase in pressure inside eye causes intense pain and blurred vision
Symptoms: nausea, vomiting, headaches, intense pain in eyes, bloodshot eyes and increased sensitivity, medium dilatation of pupil, blurred vision, coloured circles surrounded by light
What is the aim of pharmacotherapy for glaucoma?
Reduce intraocular pressure (IOP) to prevent damage to nerve fibers and prevent visual defects
1) Decrease aqueous production by ciliary body
2) Increase aqueous outflow through trabecular meshwork and uveal outflow paths
Drugs used to manage chronic glaucoma
Beta blockers
Alpha 2 agonists
Carbonic anhydrase inhibitors
Prostaglandin agonists
Parasympathomimetics
Drugs for emergency condition–closed angle glaucoma
Hyperosmotics
Note: can also use laser to puncture iris and allow outflow of aqueous humor from posterior chamber!
Drugs that inhibit aqueous humor inflow
Beta blockers (timolol (topical administraction)): block beta receptors on ciliary epithelium so Na/K ATPase can’t let Na+ into aqueous humor and thus no water osmotically moves in either
Alpha 2 agonists (brimonidine, apraclonidine (topical administration)): act presynaptically at alpha 2 receptors to inhibit NE release and also block Na/K ATPase from letting Na+ into aqueous humor and thus no water osmotically moves in either
Carbonic anhydrase inhibitors (acetazolamide (systemic) and dorzolamide (topical)): reduce HCO3- production (enzymatic process) and secretion into aqueous humor and thus no water osmotically moves in either
Drugs that increase aqueous humor outflow
Parasympathomimetics (pilocarpine, AChE inhibitors): contract ciliary muscle to increase tone and alignment of trabecular network and facilitate aqueous humor outflow via trabecular meshwork
F2alpha prostaglandin agonists (lantanoprost): increase uveoscleral outflow (aqueous humor goes between ciliary bundles and into episcleral tissues to be reabsorbed into orbital blood vessels and drained via conjunctival vessels)
Hyperosmotics
Mannitol (20% IV solution) or glycerol (50% oral solution)
Increase serum osmolarity to reduce intraocular water content by drawing water out of the eye
Use caution in congestive heart failure; avoid glycerol in diabetics
Used only in management of acute elevations of IOP as seen in closed angle glaucoma and occasionally after surgery
Optic cupping
Cuppng of optic nerve is appearance of optic nerve viewed through pupil–empty space in middle of optic nerve surrounded by nerve fibers
Glaucoma causes loss of nerve fibers and cup becomes larger (larger C/D ratio means more damage) because less space occupied by remaining nerve fibers
