Flashcards in Unit 3 - Ocular Pharmacology Deck (54):
what is the anterior segment of the eye made of?
cornea, iris, lens, and ciliary body
what is the cornea?
tough, transparent, avascular dome-like structure covering the front of the eye
-this is flattened in Lasik surgery
what is the iris?
pigmented tissue allowing transmission of central light rays through pupil
what is the pupillary aperture controlled by?
dilator and sphincter muscles within the iris
what is the lens?
pliant bag filled with protein
-as thickness changes (from muscular fibers within ciliary body via tension on zonules), it alters focal point of eye
--this is intrinsic in accommodation, allowing good vision at different distances
what is the ciliary body?
site of production of aqueous, which is the source of nutrition for lens, cornea, and trabecular meshwork
what is the trabecular meshwork?
located at peripheral edge of anterior chamber
-aqueous drains through collector channels before leaving the eye
-production must match outflow, or else intraocular pressure may rise, causing damage to optic nerve --> glaucoma
--thus TM is the worst place to have angiogenesis
what is angle closure glaucoma? how do you check for it?
flow of aqueous is prevented from draining into trabecular meshwork by iris bowing forward
-check by shining light from temporal side of eye
--if nasal iris has shadow over it, then the anterior chamber may be shallow due to bowing forward of the iris --> predisposition to angle closure
--if both temporal and nasal iris are illuminated similarly, the anterior chamber is deep (normal)
what does ambient light test show if the optic nerve is damaged in only one eye?
1. shine light on defect eye, both constrict a little (4 mm)
2. shine light on normal eye next, both constrict a lot (2 mm)
3. shine light back on defect eye, there is paradoxical dilatation of defect eye
what is convergence insufficiency?
patient can thicken lens and constrict pupils, but not converge eyes
-causes eye strain after prolonged periods of close work
what is light-near dissociation?
pupils will not constrict to bright light, but will when focusing on close object (light reflex is absent, but pupillary constriction with near vision intact)
-occurs in Parinaud's syndrome (pineal tumors), Argyll Robertson syndrome (secondary to syphillis), and Adie syndrome (benign parasympathetic deficit)
are pre or post-ganglionic problems more severe?
pre ganglionic are more severe, while post-ganglionic are more benign (migraine-like)
what is the differential diagnosis for pre-ganglionic lesions?
2. compression of nerve due to displacement of brain stem, herniation of uncus, aneurysm, tumor
3. ischemic infarct of nerve
what are the differential diagnoses for post-ganglionic lesions?
1. Adie's syndrome due to inflammation, injury, tumor, etc.
2. any other migraine-like disease
how does a parasympathetic pathway stimulate the eye?
both central and ocular origins
1. light rays stimulate photoreceptors within retina, triggering signal to fibers in optic nerve
2. decussate within chiasm, exit optic tract before LGB, and travel to brainstem at level of superior colliculus
3. synapse in pretectum where fiberes are distributed to ipsilateral and contralateral Edinger-Westphal nucleus
4. efferent fibers travel with CN III from brainstem and synapse at ciliary ganglion
5. short ciliary nerves then carry these fibers to ciliary body and iris sphincter
where are the muscarinic receptors in the eye?
for parasympathetic system
-iris sphincter (constricts pupil)
-circular fibers of ciliary muscle (constrict pupil)
-longitudinal fibers of ciliary muscle (place tension on trabecular meshwork
what are direct parasympathetic agonists for use on the eye? the effect? the use?
ACh (miochol), carbachol, methacholine, pilocarbine
-effect: pupillary constriction, increased aqueous flow
-use: after cataract surgery to ensure proper procedure, treatment of glaucoma
what are parasympathetic antagonists? their effects? use?
cycloplegics: atropine, scopolamine, homatropine, cyclopentolate, tropicamide
-effect: pupillary dilation, paralysis of ciliary body
-use: for eye exams and improve comfort during active eye inflammation (uveitis)
what are long term VS short term antimuscarinic effects?
atropine is long term (takes 7-12 days for total recovery)
tropicamide is short term (takes ~6 hours for total recovery)
what is the only ophthalmogic sympathetic agonist?
indirect nicotonic agonist to neuromuscular junction: edrophonium (diagnoses myasthenia gravis)
how does the sympathetic system affect the eye?
originates in hypothalamus
1. fibers descend downward to brainstem, uncrossed, to ciliospinal center of Budge around C8-T2
2. after synapsing, second order neurons exit spinal column to ascend with paravertebral sympathetic chain to reach superior cervical ganglion
3. fibers synapse to become third order neurons, that run with carotid plexus and join ophthalmic division of CN V
4. fibers pass with nasociliary nerve and then with long ciliary nerve to reach the ciliary body and dilator muscle of iris
where are the NE ocular receptors and what do they do/
1. iris dilator muscle (dilates pupil)
2. superior palpebral muscle of Muller (lifts eyelid)
3. ciliary epithelium (facilitates aqueous production)
4. smooth muscle of ocular blood vessels (dilates blood vessels)
5. trabecular meshwork (increases outflow of aqueous)
what is phenylephrine? what does it do?
direct NE agonist at a1 --> dilates pupil
what is L-epinephrine? what does it do?
epinal: alpha and beta agonist --> decrease ocular pressure for glaucoma
what is dipivalyl epinephrine? what does it do?
Propine; pro-drug of epinephrine to decrease ocular pressure for glaucoma
what is bromondine tartrate? what does it do?
Alphagan: selective a2 agonist to suppress aqueous humor production thru action of cAMP in ciliary
-decreases ocular pressure
what is apraclonidine? what does it do?
Iopidine: alpha agonist
-amino derivative of clonidine which doesn't cross BBB and has minimal effect on systemic blood pressure
what is clonidine? what does it do?
-lowers intraocular pressure through CNS effects
why is apraclonidine better than clonidine?
apra doesn't cross BBB thus has less effect on systemmic blood pressure
what are indirect agonists of NE for ocular?
1. cocaine - prevents reuptake of NE
2. hydroxyamphetamine (Paradrine) - releases NE
what are NE antagonists for ocular usually targeting versus agonists?
antagonists target beta 1/2, while agonists target alpha1/2
-both will decrease intraocular pressure
what is dapiprazole? what does it do?
"Rev-eyes" NE antagonist
-reverses action of tropicamide (antimuscarinic) and phenylephrine (a1 agonist) that dilate pupils
-blocks alpha-adrenergic receptors in smooth dilator muscle of iris
what is timolol? how frequently do you use it? contraindications?
Timoptic: non-specific beta 1 and 2 blocker
-use once a day
-don't use if CHF, asthma, bradycardia
--over time may produce tachyphylaxis
what is betaxolol?
Betoptic: B1 blocker (thus causes CHF but not asthma)
why do you need to be careful with B1/2 antagonists?
B1 may exacerbate CHF (inhibitory effect on heat)
B2 may exacerbate asthma (constriction of smooth muscle and bronchioles)
what is carteolol?
Ocepess; non-specific B1/2 blocker
what is Levobunolol?
Betagan: beta2 blocker
what is metipranolol?
OptiPranolol; non-selective B1/2 blocker without significant intrinsic sympathomimetic activity, only a weak membrane stabilizing activity and weak myocardial depressant
how are sympathetic and parasympathetic agents used to treat glaucoma?
sympathetic alpha agonists: increase aqueous outflow by dilating episcleral vessels
sympathetic beta antagonists: reduce aqueous production at ciliary process
parasympathomimetics: spread trabecular meshwork through ciliary muscles
these all cause reduced intraocular pressure
what are non sympathic/parasympathetic-related methods to treat glaucoma?
1. carbonic anhydrase inhibitors
2. osmotic agents
how do carbonic anhydrase inhibitors work?
interfere with active transport of Na through Na-K-ATPase pump
-can be topical or oral
-act on ciliary body to reduce production of aqueous
how do osmotics work?
interfere with passive transportation of fluid in ciliary body
-increase serum osmolarity, drawing fluid from extravascular space to intravascular space
what is the main therapy used to treat glaucoma? how do they work/
-increase uveoscleral outflow without any effect on aqueous flow or trabecular outflow facility
what is latanaprost? how frequently should you use it? contraindications?
prostaglandin analog, usd once per day
-contraindications are cystoid macular edema, herpes, eyelash growth, and change in iris color
what is brimondine? how frequently should you use it? contraindications?
alpha 2 agonist used 3 times a day
-use with MAOi can cause fatigue/drowsiness, follicular conjunctivitis
what are dorzolamide and hydrochloride? how frequently should you use it? contraindications?
carbonic anhydrase inhibitors
-use 3x a day
-don't use if allergic to sulfonamides (along with the other combo drugs)
what is nifedipine?
Ca++ channel blocker that increases ocular perfusion at nervehed without acting on ciliary body or trabecular meshwork
-used in low-tension glaucoma
how do you diagnose Horner's syndrome? what should you do afterwards?
1.. diagnose with topical cocaine, which inhibits NE reuptake and normally causes pupillary dilation
-if Horner's, sympathetic is dysfunctional, so no dilation
2. now must separate preganglionic (1st/2nd order, ominous) from postganglionc (3rd order, benign)
-use Paredrine to release NE and cause pupillary dilitation at 3rd order
--if there's dilation, that means it's a preganglionic lesion
--if there's no dilation, it's postganglionic
what will an internal carotid aneurysm do? how can you tell the difference from Adie's syndrome?
cause trauma to CN III, resulting in pupillary dilitation, since parasympathetic pathway travels with CN III
-associated extraocular muscle palsies and ptosis, as CN III supplies extraocular muscles and lid
-this is an emergency and requires immediate study; associated with headaches
-require normal doses of methacholine (10%) and pilocarpine (1%) to constrict
what is Adie's syndrome? how can you tell the difference from fatal internal carotid aneurysm?
chronic damage to ganglion that produces parasympathetic dysfunction (tonic pupil)
-dilated pupil with sector palsies of pupillary sphincter
-benign and from viral infection or trauma to ciliary ganglion (migraine-equivalent)
-pupils will constrict with low doses of methacholine (2.5%) and pilocarbine (1/8%); this is unique to AS
what are adverse effects of beta-blockers? on which organ systems?
cardiovascular: bradycardia, hypotension, syncope, palpitation, CHF
neurologic: mental confusion, depression, fatigue, lightheadedness, hallucinations, memory impairment, sexual dysfunction
what are adverse effects of adrenergics? on which organ systems?
cardiovascular: extrasystoles, palpitations, HTN, MI
miscellaneous: trembling, paleness, sweating
what are adverse effects of cholinergic/anticholinesterases? on which organ systems?
GI: salivation, N/V, diarrhea, abdominal pain, tenesmus
miscellaneous: lacrimation, sweating