Glaucoma Flashcards
What is glaucoma
Eye disease characterized by intraocular hypertension or increased pressure within the eye
At what intraocular pressure can a glaucoma be confirmed
> 22 mmHg
Why can glaucoma cause blindness or vision loss
Increased pressure in the eye can lead to damage of the optic nerve
Clear front of the eye that transmits and focuses light onto the eye
Cornea
Colored part of the eyes with muscles to constrict or relax the eye to regulate the size of the pupil
Iris
Size determines or regulates how much light enters the eye
Pupil
Transparent flexible tissue that help focus light and images on the retina
Lens
Senses light and create electrical impulse and sends them to the optic nerve
Retina
The chamber between the cornea and iris
Anterior chamber
Chamber between Iris and lens
Posterior chamber
Btw the Lens and retina carrying Virteous humor
Virteous Chamber
What chambers carry the aqueous humor
Anterior and posterior chamber
Clean water fluid produced by the ciliary body and brings nutrient to the eyes and maintains intraocular pressure
Aqueous humor
What is the roadway travel of aqueous humor
Starts from the posterior chamber to the anterior chamber through the pupil, across the iris and trabecular meshwork into the collecting duct (canal of schlemms) to the episcleral vein
What happens when aqueous humor enters the episcleral vein
It is absorbed into the bloodstream
What causes the intraocular pressure that leads to glaucoma
Interruption in flow of aqueous humor as a result of a blockage
Once blindness or damage to the optic nerve occurs is there treatment
No
What is the goal of glaucoma therapy
Prevent further damage to the optic nerve
What are the risk factors of glaucoma
Older adults
Family history of glaucoma
African Americans
Systemic or topical corticosteroid use
Patients with high intraocular pressure
Diabetes
Myopia
Genetic mutations
Thinner central corneal thickness
What is primary open angle glaucoma
Blockade in the trabecular meshwork causing increased resistance to aqueous humor drainage through the trabecular meshwork
What is primary closed angle glaucoma
Increase in the lens size that it presses against the cornea leading to obstruction of drainage pathways by the Iris
What are the diagnostic test
Visual field testing
Ocular tonometry
Open angle glaucoma symptoms
Asymptomatic until substantial vision loss occurs
Reduce IOP by 20-30% to reduce risk of optic nerve damage
True/False: in open angle glaucoma Intra ocular pressure can be normal or elevated ( > 21 mmHg)
True
In open angle glaucoma what is considered mild IOP
Optic disk abnormalities with normal visual field
In open angle glaucoma what is considered moderate IOP
Optic disk changes with visual field abnormalities in one hemifield
In open angle glaucoma what is considered severe IOP
Optic disk changes with visual field abnormalities in both hemifield
Open angle glaucoma signs
Disk changes and visual field loss
Closed angle glaucoma symptoms
Asymptomatic
Prodromal symptoms
Acute episodes
Prodromal symptoms of closed angle glaucoma
Blurred vision
Halos around light
Occasional headache
Acute episodes of closed open Glaucoma
Cloudy
Edematous corneas
Ocular pain
Discomfort
Nausea and vomiting
Abdominal pain
Diaphoresis
What are the signs of closed angle glaucoma
Acute
Hyperemia Conjuctiva
Cloudy cornea
Shallow anterior Chamber
Occasional edematous and hyperemic optic disk
True/False: Closed angle glaucoma IOP is generally markedly elevated (40-90mmHg)
True
Which drugs induce open angle Glaucoma
Corticosteroids
Ophthalmic anticholinergics
Succinylcholine
Vasodilator
Cimetidine
Drugs that induce closed angle glaucoma
Anticholinergics
BZ
Topiramate
Antihistamine
Tetracycline
Pratropium
Phenothiazine
SSRIs
Venlafaxine
Sympathomimetics
How are ways in which IOP is decreased
Decrease aqueous humor production
Increase aqueous humor outflow
Both ways
Drugs to decrease aqueous humor production
Beta-blockers
Carbonic hydrase inhibitors
Drugs to increase aqueous humor outflow
Prostaglandin analogs
Cholinergic analogs
Rho kinase inhibitors
Drugs of both ways
Alpha 2 adrenergic agonist
Beta blockers cap color
Yellow
Beta blocker MOA
Decrease production of aqueous humor by the ciliary body
Non-selective beta blockers
Timolol
Levobunolol
Metipranolol
Carteolol
Selective beta blocker
Betaxolol
Reduce IOP by 20-30%
Beta blockers
Frequency of beta blocker administration
BID
Systemic ADR of beta blockers
Decreased heart rate
Decreased blood pressure
Bronchospasm
Local adp of beta blockers
Ocular irritation and dry eyes
Carbonic anhydrase inhibitors cap color
Orange
Topical CAI
Dorzolamide
Brinzolamide
CAI MOA
Inhibit aqueous humor production by blocking active secretion of sodium and bicarbonate ions from the ciliary body
Systemic CAI is typically reserved for?
Acute treatment
Reduce CAI by 15-26%
CAI
CAI Frequency of Dosing
BID or TID
CAI local ADR
Burning or stinging
Dry eyes
Ocular discomfort
Transient blurred vision
Tearing
CAI Systemic ADR
Malaise
Fatigue
Nausea
Weight loss
Altered taste
Renal stones
What color are prostaglandin analog color
Blue
Drugs of prostaglandin analogs
Bimatoprost
Lantanoprost
Tafluprost
Travoprost
Lantanoprostene bound
Prostaglandin analog MOA
Increases uveoscleral outflow and trabecular outflow of aqueous humor
Produces collagen changes in the matrix of the cilliary body and trabecular meshwork
Lantoprostene bunod
Latanoprost prodrug metabolized to nitric oxide donating moiety
Reduce IOP by 25-35%
Prostaglandin Analogs
Frequency of prostaglandin analog dosing
Once daily
One drop at night
Local ADR of prostaglandin analogs
Lengthening and darkening of eyelashes
Brown discoloration of eyes (irreversible)
Macular edema
Systemic ADR of prostaglandin analogs
Minimal but may occasionally cause headache
Cholinergic agent cap color
Green
Drugs of cholinengic cholinergic agents
Pilocarpine
Carbachol
Cholinergic agent MOA
Physical pulling of trabecular meshwork open thereby increasing outflow
IOP reduction by 20-30%
Cholinerigic agents
Cholinergic dosing frequency agents
TID or QID
Local ADR of cholinergic agents
Mitosis: decreasing vision and night vision IM patients with central cataracts
Ocular discomforts
Systemic ADR of cholinergic agents
Frontal headache
Brow ache
Eyelid twitching
Rho kinase inhibitor
Netarsudil
Netarsudil MOA
Increases trabecular meshwork outflow
Decrease IOP by 15-22%
Netarsudil
Frequency of Netarsudil dosing
Once daily
Local ADR of Netarsudil
Conjunctival hyperemia and hemorrhage
Corneal verticillate
Systemic ADR of Netarsudil
Rare
How can we increase outflow and decrease production
Alpha 2 adrenergic agonist
Drugs of alpha 2 adrenergic
Bromonidine
Apraclonidine
Reduce IOP by 18-27%
Alpha 2 adrenergic agonist
Frequency of Dosing of alpha 2 adrenergic agonist
BID or TID
Local ADR of alpha 2 agonist
Allergic reactions
Dry eyes
Ocular discomfort
Systemic ADR of alpha 2 agonist
Dizziness
Fatigue
Dry mouth
Reduction in blood pressure and pulse (postural hypotension)
Who should alpha 2 be dosed cautiously
Patient with insufficient coronary and cerebral function
Hepatic and renal dysfunction
Timolol combination drop
Dorzolamide
Brimonidine
Prostaglandins
Brimonidine combo.
Brinzolamide
Netarsudil combo
Lantanoprost
First line therapy
Prostaglandin analogue
Beta blocker
Alternate first line
Brominidine
If there is contraindication to first line therapies what should be used
Topical CAI
How long till patient is reassessed
2-4 weeks
If patient is intolerant fo therapies what should be done
Reduce dose/concentration first
Or
Change formulation
Or
Switch to Class alternative or alternative combination
If inadequate response what should be done
Ensure compliance
Instruct on nasolacrimal occlusion
Increase concentration or dose frequency
Switch to alternative first line therapies
If partial response with first line agents what should be done
Add second or third first line agent or topical CAI
If there is inadequate response to first line and second line what should be done
Consider adding direct-acting cholinergic agent as fourth line and consider replacing with cholinestrase inhibitor
Consider adding oral CAI over topical CAI
Multiple topical therapies plus oral carbonic anhydrase inhibitor
When all pharmanologic therapy have failed that is left to do
Surgery or laser procedure
Surgery for open angle glaucoma
Trabeculoplasty
Surgery for closed angle glaucoma
Iridofomy
What is acute angle closure crisis (AACC)
Medical emergency: sudden closure of angle between the iris and trabecular meshwork lending to rapid increase of IOP
Symptoms of AACC
Rapid onset of blurred vision
Red eye
Pain
Headache
Nausea and vomiting
Goals of therapy for AACC
Rapidly Reduce IOP
Avoid surgical or laser iridectomy
AAC treatment options
One or more anti-glaucoma agent:
Miotics-pilocarpine
Secretory inhibitors: beta blockers, alpha I agonist, topical/systemic CAI
or
Prostaglandins
Give osmotic agents like oral glycerin 1-2 g/kg or IV mannitol 1-2 g/kg
Quickly withdraw water from the eyes using osmotic gradient between the blood and eye
When all pharmacologic therapies for AACC fail what should be done.
Peripheral iridectomy
What should patients know prior to Administration
Do not administer more than one drop per dose
When 2 or more drugs administered, meds should be separated by at least 5 minutes (10 minutes
preferred)
Remove contacts prior to administration
Systemic CAI
Acetazolamide
Dichlorphenamide
Methazolamide