Pharm U3 optho. Flashcards
what allows transmission of central light rays through the pupil?
iris
pupillary aperture is controlled by what?
dilator and sphincter muscles
what is the lens?
pliant bag filled with protein
what is the lens thickness controlled by?
muscular fibers within the ciliary body via tension on the zones
accommodation
ability to alter the focal point
where does production of aqueous happen?
ciliray body
what is aqueous
source of nutrition for the lens, cornea, and trabecular meshwork
gluacoma
when intraocular pressure rises causing damage to the optic nerve due to aqueous production being more than aqueous outflow
angle closure glaucoma
flow of aqueous is prevented from draining into the trabecular meshwork by bowing forward of the iris
trabecular meshwork
located at the peripheral edge of the anterior chamber
how to test for predisposition of angle closure glaucoma
penlight - if both temporal and nasal iris are illuminated similarly - anterior chamber is deep. if nasal iris has a shadow over it, then the anterior chamber may be shallow due to bowing forward of the iris
sympathetic system causes what of the eye?
dilation of pupil
what syndromes demonstrate pupils not constricting to bright light but constricting when focusing?
parinaud’s syndrome (pineal tumor), argyll robertson syndrome (syphilis), Adie syndrome (benign parasympathetic deficit)
parasympathetic system causes what?
pupillary constriction
what controls modification of lens thickness and aqueous production
ciliary body
how is sympathetic innervation of the eye transmitted?
adrenergic receptors via NE - alpha and beta receptors
how is parasympathetic innervation transmitted?
cholinergic receptors via acetylcholine
what receptors are present in the eye for parasympathetic innervation
muscarinic and nicotinic
muscarinic receptors are block by what?
atropine
nictonic receptors are blocked by what?
d-tubocurarine
nicotinic receptors on the eye are found where?
extraocular muscles
muscarinic receptors for the eye are found where?
ciliary body and iris
muscarinic receptors action on eye
iris sphincter constrict pupil, circular fibers of ciliary muscle to constrict pupil, and longitundinal fibers of ciliary muscle to place tension on trabecular meshwork
Muscarinic agonists and their effects
acetylchoine, carbachol, methacholine, pilocarpine. cause pupillary constriction and increased aqueous outflow
when are muscarinic agonists used
cataract surgery and glaucoma treatment
muscarinic antagonists and their effects
atropine, scopolamine, tropicamide. pupillary dilatation and paralysis of ciliary body
when are muscarinic antagonists used
cycloplegia for eye exams and to improve comfort during active eye inflammation (uveitis)
what are the ACE inhibitors
echothiophate (irreversible) and physostigmine
what is the nicotinic agonist? when is it used
edrophonium - used to diagnose myasthenia gravis
describe the path of the sympathetic system from origin to eye
hypothalamus -> brainstem -> synapse to become second order and ascend with paravertebral sympathetic chain -> synapse at superior cervical ganglion to become third order neurons -> run with carotid plexus and run with ciliary nerve (V) to reach ciliary body and dilator muscle of the iris
what are the direct sympathetic agonists? what receptor do they effect?
phenylephrine (mimic NE alpha 1- dilation of pupil); bromondine tartrate (selective a-2 agonist which suppresses aqueous humor production); clonidine (alpha-adrenergic agonist - lowers intraocular pressure through CNS effects)
what are the indirect sympathetic agonists? what effect do they have
cocaine (prevent reuptake of NE) and hydroxyamphetamine (paradrine - releases NE)
what are the sympathetic antagonists? what receptor do they effect?
beta blockers (-olol) timolol (non-specific beta 1 and 2) and betaxolol (beta 1 blocker, avoiding pulmonary symptoms)
which drug reverses action of tropic amide and phenylephrine?
dapiprazole
what are the first line medications for glaucoma?
timolol (non-specific beta-blocker), Latanaprost (prostaglandin), brimondine (alpha 2 agonist), dorzolamide hydrochloride (carbonic anhydrase inhibitor)
carbonic anhydrase inhibitor mechanism and drug used
dorzolamide hydrochloride - topical - interfere with the active transport of Na through Na-K-ATPase pump
what is the mechanism of prostaglandin analogs? drug used?
increase uveoscleral outflow without any effect on aqueous flow or trabecular outflow facility - Latanoprost (effective in reducing intraocular pressure)
How is Horner’s syndrome diagnosis confirmed?
cocaine - if sympathetic system is dysfunctional, pupillary dilatation will not occur
how is the location of the abnormality in horner’s syndrome confirmed?
paredrine (hydroxyamphetamine) - if the pupil does not dilate with paredrine, then the 3rd order neuron is dysfunctional (benign)
What does loss of parasympathetic innervation cause?
disruption of the balance with the sympathetic system effecting pupillary innervation resulting in dilatation of the pupil
which syndromes cause pupillary dilatation through loss os parasympathetic innervation in the eyes?
intracranial aneurysms, Adie’s syndrome, pharmacologic blockade
how does internal carotid aneurysm result in pupillary dilatation?
trauma to the 3rd nerve from the aneurysm with associated extra ocular muscle palsies and ptosis, also occur with headaches
Adie’s syndrome
damage to ciliary ganglion - characterized by dilated pupil with sector palsies of the pupillary sphincter - benign (due to viral infection/trauma)
How to tell the difference between Adie’s syndrome and internal carotid aneurysm
a small dose of Ach will stimulate a chronically denervated nerve in Adie’s but not a traumatized nerve (aneurysm). normal eye needs 1% pilocarpine or 10% methacholine to cause constriction. In adie’s - only need 1/8% pilocarpine or 2.5% methacholine to cause pupillary constriction
how can you tell if pupillary dilation is due to pharmalogic blockade? which drugs cause this?
pilocarpine 1% does not constrict pupil - caused by cycloplegic agents (muscarinic antagonists blocking action of actylcholine)
beta blockers adverse effects
cardio (bradycardia, hypotension, syncope, CHF) resp (bronchospasm) neurologic (confusion, depression, fatigue, hallucinaions)
adrenergics adverse effects
cardio (extrasystoles, palpitation, hypertension, MI) along with tremblinc, paleness, sweating
cholinergic/anticholinesterases adverse effects
respiratory (bronchospasm), GI (salivation, nausea, vomiting, diarrhea, ab pain) also lacrimation and sweating
anticholinergic adverse effects
neuro (ataxia, nystagmus, restlessness, confusion, hallucination, aggressive behavior) and also insomnia, photophobia, urinary retention
