Glaucoma Meds Flashcards
What causes the pupil to constrict?
iris circular muscle
M3 receptor
What causes the pupil to dilate?
iris radial muscle
alpha 1
What causes accommodation of the eye to near vision and decreases intraocular pressure (improves outflow of aqueous humor)?
ciliary muscle
M3
What produces aqueous humor?
ciliary epithelium
What activation increases humor production?
beta adrenergic
What receptor activation decreases humor production?
alpha 2
What does carbonic anhydrase do to aqueous humor?
transports sodium and bicarb from ciliary body into humor
increases osmotic pressure, enhances water transport to humor–>increases volume
What improves outflow of aqueous humor?
contraction of ciliary muscle
contraction of iris circular muscle (constriction of pupil)
both M3
What improves unconventional aqueous humor outflow?
prostaglandin F2a
What does sympathetic nervous system do to eye?
dilates pupil via contraction of iris radial muscle (decrease outflow)
–> alpha 1
relax ciliary muscle (increase uveoscleral outflow)
–> alpha 2
Define glaucoma
ocular disorders–> optic neuropathy a/w loss of visual sensitivity and field
What types of glaucoma are there?
primary (genetic, congenital)
- -> open angle glaucoma most common: progressive disease without mechanical blockage to humor outflow
- -> closed angle glaucoma: acute intermittent partial or complete blockage of outflow (emergency to avoid vision loss)
secondary (disease, trauma, surgery, drug-induced)
What is the most common form of glaucoma?
open-angle (no known outflow blockage)
What is one factor that can cause open angle glaucoma?
increased IOP–> optic neuropathy (damage to optic nerve)
Generally, what drugs reduce the amount of aqueous humor produced?
beta blockers (olol)
alpha 2 agonists (idine)
carbonic anhydrase inhibitors (amide)
Generally, what drugs increase aqueous humor outflow?
prostaglandin analog (oprost)
alpha 2 agonist (idine)
direct cholinergic agonist
inhibitors of cholinesterase
Why is Timolol favored in glaucoma?
lacks local anesthetic effects
generic
full antagonist
Why are beta blockers used?
convenience of dosing
general lack of local adverse effects
Beta blocker MOA
reduce production of humor by ciliary body
Local adverse effects of beta blockers
little, usually well tolerated
ocular irritation
dry eyes
Systemic adverse effects of beta blockers
bradycardia
bronchospasm
hyperlipidemia
hypoglycemia
interact with calcium blockers
careful with use in cardiac patients
What is the main alpha 2 agonist used in glaucoma?
brimonidine
Alpha 2 agonist MOA
decrease humor production
increase uveoscleral outflow (unconventional) via relaxing ciliary muscle
Side effects of alpha 2 agonists
systemic: headache, fatigue, dry mouth
local: eyelid edema, itching, hyperemia (allergic rxn)
MOA of carbonic anhydrase inhibitors
-lamide
decrease osmotic pressure of humor
Side effects of carbonic anhydrase inhibitors
local–> ocular irritation and redness
systemic: N, diarrhea, altered taste, weight loss, paresthesia, renal stones, decreased libido
intolerable with long-term use
MOA of prostaglandin analogs
-oprost
reduce IOP via increased uveoscleral and conventional outflow of humor
Why give prostaglandin analogs for glaucoma?
once at nighttime
more efficiently reduce IOP c/t beta blockers
Adverse effects of prostaglandin analogs
systemic not significant
local: corneal erosions, hyperemia, iris hyperpigmentation (irreversible with months of use), hypertrichosis of eye lashes that is reversible with d/c
What are direct-acting cholinergic agonists?
pilocarpine
carbachol
What are indirect-acting cholinergic agonists (AKA inhibit cholinesterase)?
echothiophate
MOA of cholinergic agonists
activate M3 directly or indirectly (inhibit cholinesterase)–> elevate Ach levels
increases conventional humor outflow
Adverse effects of cholinergic agonists
systemic rare
local: ha, periorbital pain, constriction of pupil with diminished night vision, eyelid twitching, myopia, cataracts with long-term use, iris-lens adhesions with long-term use
How to treat glaucoma
beta blocker or prostaglandin first
if intolerant: use class alternative
if contraindications to both: brimonidine or topical carbonic anhydrase inhibitor
combo therapy
laser or surgical procedure
Describe pupillary block closed angle glaucoma
tight contact between iris and lens–> flow of humor into anterior chamber blocked–> iris moves forward and blocks outflow
Describe closed angle glaucoma without pupillary block
ciliary processes located in such a way that they push the iris forward–> blocks outflow, especially when pupil is dilated
Goals for treatment of closed angle glaucoma
medical emergency to keep vision
- -> reduce IOP with oral glycerin or IV mannitol to prep for surgery
- -> pilocarpine before surgery induces constriction of pupil
- -> reduce humor production via beta blocker, alpha 2 agonist or carbonic anhydrase inhibitor
What drugs promote elevation of IOP?
open angle glaucoma patients: glucocorticoids, topical antimuscarinic drugs
closed angle glaucoma patients, cause dilation of pupil: alpha 1, antimuscarinic drugs
