Ocular Pharm Flashcards
Cornea is a
tough, transparent, avascular dome-like structure covering the front of the eye
Iris is the
pigmented tissue allowing transmission of central light rays through the pupil; pupillary aperture controlled by dilator and sphincter muscles within the iris
As the lens changes thickness, it will; thickness controlled by
alter the focal point of the eye; muscular fibers within ciliary body via tension on the zonules
Ability to alter focal point is
intrinsic in accommodation, allowing good vision at different distances
Ciliary body is
site of production of aqueous; serves as source of nutrition for lens, cornea, and trabecular meshwork
Angle closure glaucoma occurs when
flow of aqueous is prevented from draining into trabecular meshwork by bowing forward of the iris
If anterior chamber is deep,
temporal and nasal iris illuminated similarly; anterior chamber could be shallow if nasal iris has shadow over it
For accommodation to work, what mechanisms are needed?
- Thickening of the lens
- Convergence of the eyes
- Pupillary constriction;
With numbers 1 and 3, but 2 not working, you could have convergence insufficiency
Muscaranic receptors can be blocked by what? Nicotinic receptors can be blocked how?
Atropine; d-tubocurarine
In the eye the nicotinic receptors are found in _____; the muscarinic receptors are in the
extraocular muscles;
ciliary body and iris!!
Outline the parasymp pathway going from light rays to innervation of the ciliary body and iris sphincter
- Light rays hit photoreceptors within retina, triggering signal to fibers in optic nerve
- Fibers decussate within chiasm and exit optic tract PRIOR to LGN
- Travels to brainstem at level of superior colliculus
- Synapse in pretectum and fibers go to ipsilateral and contralateral EW nucleus
- Efferent fibers travel with CN III from brainstem and synapse at ciliary ganglion
- Short ciliary nerves carry fibers to ciliary body and iris sphincter
What’s an NT for muscarinic receptors? List some agonists and antagonists and their effects and uses
NT = ACh, receptor = muscaric,
muscarinic receptors: iris sphincter (constrict pupil), circular fibers of ciliary muscle (constrict pupil), longitudinal fibers of ciliary muscle (place tension on trabecular meshwork)
Agonists: direct (ACh, carbachol, methacholine, pilocarpine); EFFECT: pupillary constriction, increased aqueous outflow; USE: cataract surgery, treatment of glaucoma
Antagonists: atropine (takes longer to recover), scopolamine (a little less time than atropine to work and recover), homatropine (quicker recovery time), cyclopentolate (shorter recovery time than first three), tropicamide (shortest recovery time); EFFECT: pupillary dilation and paralysis of ciliary body; USE: cycloplegia for eye exams and to improve comfort during active eye inflamm (uveitis)
Symp system originates where and finishes where?
- Hypothalamus origin and fibers descend to brainstem, uncrossed, to ciliospinal center of Budge around C8-T2
- Synapses and second order neurons exit spinal column and ascend with paravertebral symp chain to reach superior cervical ganglion
- Fibers synapse again and become third order neurons
- Third order neurons run with carotid plexus and join ophthalmic division of CN V
- Fibers pass with nasociliary nerve and with long ciliary nerve to reach CILIARY BODY and dilator muscle of iris!!
In symp system, what’s the main NT? What receptors are used?
NT = NE;
receptors: alpha 1 (smooth muscle contraction), alpha 2 (feedback inhibition of presyn symp), beta 1 (stimulatory effect on heart), beta 2 (relaxation of smooth muscle in bv’s and bronchi);
ocular receptors: iris dilator muscle (dilate pupil), superior palpebral muscle of Muller (lifts eyelid), ciliary epi (facilitates aqueous production), smooth muscle of ocular bv’s (dilates bv’s), trabecular meshwork (increase outflow of aqueous)
Agonists in symp system?
Direct: phenylephrine (mimic NE alpha 1 to dilate pupil), L-epinephrine: alpha and beta agonists for glaucoma, dipivalyl epi: prodrug of epi; bromondine tartrate (selective alpha-2 agonist to suppress aqueous humor/prduction), clonidine (alpha-adrenergic agonist, lowers IOP through CNS effects)
Indirect: cocaine (prevent reuptake of NE), hydroxyamphetamine (release NE)
Antagonists in symp system?
Dapiprazole (reverse action of tropicamide and phenylephrine, block alpha-adrenergic receptors in smooth dilator muscle of iris)
Timolol (non-specific beta 1 and 2), betaxolol (beta 1 blocker where you worry about CHF as SE), carteolol (non-specific beta 1 and 2), levobunolol (beta 2 blocker), metipranolol (non-selective beta 1 and 2 blocker without significant intrinsic sympathomimetic activity and only weak membrane stabilizing activity and weak myocardial depressant)
List carbonic anhydrase inhibitors and what their mechs and/or SE’s are
Acetazolamid, ethoxzolamide, and methazolamide given ORALLY (interfere with active Na transport through Na/K ATPase) but MANY SE’s;
Dorzolamide hydrochloride and brinzolamide are TOPICAL carbonic anhydrase inhibitors; SE’s are ocular and include red eyes and lid allergies
Timolol contraindication? What are types of latanaprost, brimondine, dorzolamide hydrochloride?
CHF, asthma, bradycardia;
latanaprost: prostaglandin inhibitor effective in reducing IOP: think growth of eyelashes and change in iris color, cystoid macular edema;
Brimondine: alpha 2 agonist: maybe drowsiness with MAO inhibitor and follicular conjunctivitis
DH: carbonic anhydrase inhibitor: sulfa allergies!!
In Horner’s, list things that can help confirm diagnosis?
- Cocaine given and pupil fails to dilate; if issues at pregang, give paredrine and abnormal pupil can cilate (like normal), but if POSTGANG, give paredrine and abnormal pupil will NOT dilate (normal DILATES)
How do you detect aneurysms?
Trauma to 3rd nerve from internal carotid aneurysm will result in PUPILLARY DILATION; also extraocular muscle palsies and ptosis; also look for HEADACHES!!
How do you see Adie’s syndrome?
Damage to ciliary ganglion produces parasymp dysfunction; look for dilated pupil with sector palsies of pupillary sphincter (viral infection or trauma to ganglion);
differentiate from aneurysm because ACh given will stimulate a chronically DENERVATED nerve seen in Adie’s, and not an acutely traumatized nerve from an aneurysm; if you give Adie’s patients methacholin at 2.5% or .125% pilocarpine, you can get pupillary constriction to confirm diagnosis!!
What would we see with pharmacologic blockade?
Even if you give pilocarpine 1%, you will see NO CONSTRICTION; meaning patient has been on some cycloplegic agent to block action of ACh
In a patient with glaucoma and you give you meds, what can happen?
Get headache because of stimulation of the ciliary muscle;
can also get pupillary miosis because of sphincter muscle of iris innervated
Beta blocker SE’s?
Cardiovascular: bradycardia, hypotension, syncope, CHF
Respiratory: bronchospasm
Adrenergic SE’s?
Cardiovascular: extrasystoles, palpitation, HTN, MI
Cholinergic/anticholinesterases (pilocarpine, echothiophate):
Respiratory (bronchospasm)
GI: salivation, nausea, vomiting, diarrhea, abdo pain, tenesmus (SLUDGE)
Anticholinergic (atropine)
Neurologic: ataxia, nystagmus, restlessness, mental confusion, hallucination, violent
Misc: insomnia, photophobia, urinary retention
Parinaud’s syndrome:
light-near association (think pineal tumor in kids and extensive spread of tumor); see convergence retraction nystagmus, lid retraction, limitation of upgaze
Argyll Robertson syndrome:
think tertiary syphilis, encephalitis, MS, neurosarcoidosis, lyme;
miotic irregular pupils who don’t respond to cycloplegics in a patient with good visual acuity
Other conditions to give rise to light-near dissociation?
- Injury to retina
- Optic nerve or chiasm
- Aberrant 3rd nerve regen
- Severe diabetes
Acetylcholine (Miochol): Mech and thera?
Mech: Pupillary constriction
Thera: Used in cataract surgery to constrict pupil intraoperatively
Pilocarpine HCl (Salagen)
Mech: Pupillary constriction, increased aqueous outflow
Thera: Treatment of glaucoma (both open angle and acute closed angle); used less today due to side effects
Important SE’s: Decreased vision when patient has cataracts due to miosis and headache
Carbachol
Mech: Pupillary constriction, increased aqueous outflow
Thera: Treatment of glaucoma; used less today due to side effects
Important SE’s: Decreased vision due to miosis and headache
Atropine: thera:
Improve discomfort during active eye inflammation (ueveitis)
Scopolamine: thera
Improve discomfort during active eye inflammation (ueveitis)
Homatropine
Thera: Cycloplegia for eye exams, improve discomfort during active eye inflammation (ueveitis)
Cyclopentolate: thera
Cycloplegia for eye exams, improve discomfort during active eye inflammation (ueveitis)
Tropicamide (Mydriacyl)
Thera: Most commonly used cycloplegia for eye exams
Ephinephrine
Mech: Dilation of episcleral vessels –> increased aqueous outflow
Other SE’s: Extrasystoles, palpitation, hypertension, myocardial infarction, trembling, paleness, sweating
Dipivefrin HCl (Propine)
Mech: Prodrug of epinpehrine
Thera: Treatment of glaucoma
Hydroxyamphetamine (Paredrine)
Class: Indirect adrenergic agonist
Mech: Release NE
Thera: Separates 1st and 2nd from 3rd order neuron dysfunction in Horner’s syndrome; positive dilation means 1st or 2nd order, an ominous sign
Cocaine
Class: Indirect adrenergic agonist
Mech: Prevent reuptake of NE
Thera: Use initially to confirm diagnosis of Horner’s Syndrome
Apraclonidine (Iopidine)
Class: Direct α-agonist
Mech: Amino derivative of clonidine; does not cross blood-brain barrier –> minimal effect on systemic blood pressure
Thera: Treatment of open angle glaucoma
Phenylephrine (Neo-Synephrine)
Class: Direct α1-agonist
Thera: Dilate pupil for eye exam and cataract surgery
Other SE’s: Extrasystoles, palpitation, hypertension, myocardial infarction, trembling, paleness, sweating
Misc: Caution in elderly patients: at 10% can cause cardiac side effects
Clonidine (Catapres)
Class: Direct α2-agonist
Mech: Lowers intraocular pressure through central nervous system effects
Brimondine tartrate (Alphagan)
Class: Direct α2-agonist
Mech: Suppresses aqueous humor production through action of cAMP in non-pigmented ciliary epithelium
Thera: Primary agent for treatment of glaucoma
Misc: May cause follicular conjunctivitis; use with MAOi can cause fatigue/drowsiness
Dapiprazole
Class: α-antagonist
Mech: Blocks alpha-adrenergic receptors in smooth dilator muscle of iris
Thera: Reverses tropicamide, phenylephrine
Timolol (Timoptic)
Levobunolol (Betagan)
Metipranolol (OptiPranolol)
Carteolol (Ocupress)
Class: beta-blockers
Mech: Reduce intraocular pressure by reducing aqueous production at the ciliary process (except metipranolol: Non-selective β1+2 blocker without significant intrinsic sympathomimetic activity (weak membrane stabilization, weak mycoardial depressant))
Thera: Second line treatment of glaucoma
Other SE’s: “Bradycardia, hypotension, syncope, palpitation, congestive heart failure, bronchospasm, mental confusion, depression,
fatigue, lightheadedness, hallucinations, memory impairment, sexual dysfunction, hyperkalemia”
Misc: Timolol: Contraindicated in CHF, asthma; bradycardia over time may produce tachyphylaxis
Betaxolol (Betoptic)
Class: β1-blocker
Mech: Reduce intraocular pressure by reducing aqueous production at the ciliary process
Thera: Second line treatment of glaucoma
Latanoprast (Xalatan)
Travoprost (Travatan)
Bimatoprost (Lumigan)
Class: Prostaglandin analog
Mech: Increase uveoscleral outflow
Thera: Primary agent for treatment of glaucoma
Important SE’s: Eyelash growth, change in iris color, intraocular inflammation
Misc: May cause cystoid macular edema in cataract surgery and activate herpes
Unoprostone isopryl (Rescula): differences from other three
Thera: glaucoma
Misc: least effective overall
