Glaucoma Flashcards
aqueous humor (AH) purpose
maintain proper IOP, prevent corneal collapse and optic nerve damage transparent medium for optical system nutrient delivery waste removal immune response
AH pathway
produced in ciliary body
secreted into posterior chamber
pressure from production pushes AH into anterior chamber
AH is drained and returned to circulation
AH outflow %s
90% is from trabecular outflow
10% from uveoscleral outflow through the face of the ciliary body
only modoficable RF for glaucoma
inc IOP
IOP
normal, high
normal is 13-21
>21 is elevated
normal IOP and (+) glaucomatous changes
Normotensive glaucoma (N-T)
normal IOP and (-) glaucomatous changes
normal
elevated IOP and (+) glauc changes
Glaucoma
Primary open angle (POAG) or closed angle
elevated IOP and (-) glauc changes
ocular hypertension
POAG risk factors (9)
elevated IOP (16 to 21mmHg is a 16x inc risk)
age (>60, >40 for black patients)
inc cup-to-disc ratio (0.3 +)
central corneal thickness (the thinner the worse it is)
ocular perfusion pressure (SBP or DBP - IOP –> lower = more risk)
T2DM
myopia (20/50) (near-sighted)
who should be treated
- all pts with elevated IOP and confirmed disc changes/field defects (POAG)
- OH AND 2+ RFs such as ethnicity, FHx, thin central cornea, large cup-to-disc ratio, IOP >25
- NTG with documented progressoin of visual field loss
goals of glaucoma tx
- Preserve the nerve!
2. lower IOP, target is a >/= 25% decrease
medical vs surgical tx
CIGTS study: surgery more effective at lowering IOP and better for severe cases; QOL differences w few surgical complications but possible cataract formation and loss of visual acuity
medical therapy can be as good as surgical!
tx options for POAG
prostaglandin analogs BBs alpha-antags carbonic anhydrase-i (CA-i) Rho kinase inhibitors
PG analogs
drugs
effectiveness
preferred in .... - efficacy - burning/stinging/hyperemia - generic avail use?
bimatoprost
latanoprost
latanoprostene bunod
all reduce IOP 25-35% (only one to do this adequately)
efficacy: Bimato = latano B
AE: Latano = Latano B
generic: Bimato 0.3%, Latano, Travo
1st line in all patients except ocular infections or chronic uveitis
Bimatoprost is generic at ____ concentrations BUT _____
high
increased AE :/
PG analogs AE
CI
conjunctival hyperemia, hypertrichosis, periocular/iris pigmentation changes
CI in existing ocular inflammation (keratitis, iritis, uveitis, macular edema)
BBs
MOA
drugs
preferred in convenience, systemic AE risk, generic availability?
dec AH production, minimal effects on uveoscleral outflow
betaxolol, carteolol, levobunolol, metipranolol, timolol
convenience: LVB, TIM qd sol, gel
side effect risk: BTX», CAR (for pts w/ BB CI)
generic avail: BTX sol, TIM, CAR, LVB, MTP
BBs AE
CI
local irritation (switch product/form)
systemic: cardiac, pulmonary, CNS
tachyphylaxis (20-25%)
CI: sinus bradycardia, heart block, HF (absolute), pulmonary disease (relative)
a-agonists
MOA
drug
Brimonidine
reduces AH production by ciliary body
reduces IOP 20-25% and proposed neuroprotective effect
Brimonidine AE and precautions
AE: local irritation, conjunctival hyperemia, irritation, allergic rxns
systemic: drowsiness, xerostomia, tachyphylaxis
precaution in CV diseases
Brimonidine-Timolol combo vs Latano
Iop reductions no different
diurnal control similar
latanoprost is far cheaper rn anyway
carbonic anhydrase-i
MOA
drugs
use
dec AH prod by dec bicarbonate ion secretoin reduce IOP 15-20% favorable AE profile acetazolamide (po) dorzolamide brinzolamide methazolamide (po) used as add on since dec in IOP not at 25% dorzolamide/timolol available (DTFC)
if a pt is on Bimatoprost and is having AE, want to swtich to a non PG analog… which drug should they switch to
DTFC
Rhok-i
MOA
drugs
AE
improves trobecular outflow by decreasing actin myosin contractions
~20% dec in IOP IF IOP is <27mmHg
Netarsudil (Rhopressa)
AE: high rate… , hyperemia, conjunctival hemorrhage
POAG 1st line options
PG analogs, alternative is BBs
POAG 2nd line options
dorzolamide (DTFC)
Brimonidine (alt 1st line too)
Brinzolamide, dorzolamide alone or po CA-is
netarsudil
EMGT study RF for progression
- high baseline IOP
- older age
- disc hemorrhage
- larger cup-to-disc ratio
- thinner central cornea
- low ocular perfusion pressure
- poor medication adherence
- progression in fellow eye
Ocular HTN
who to tx?
O HTN with RF
N-T glaucoma
description
tx?
wnl IOP + glocamotous changes
tx helps w sx even if its wnl
tx if NTG + documented progressoin of visual field loss
PACG
stands for?
patho?
primary angle closure glaucoma
patho:
1. pupillary block (lens contracts iris at pupillary margin
2. plateau iris (less common)
PACG attacks
when to go to hospital?
subacute attacks are self-limiting
normal/high IOP with infrequent acute angle closure crisis (AACC) GO to hopsital
AACC
definition
RF?
acute angle closure crisis
wild IOP fluctuations (up to 80mmHg)
rapid vision damage
halo around light, edematous cornea, pain, HA, N/V, rapid mydriasis
RF: shallow anterior chamber depth, FHx, hyperopia, age
AACC goal
medically break the attack quickly to preserve vision and prep eye for laser peripheral iridotomy (LPI)
AACC treatment IOP
CA-i (500mg acetazolamide IR IV or po)
topical BB
topical alpha-ag
AACC treatment angle
AE
topical pilocarpine
induces miosis
AE: spasm, HA, brow ache, lid twitch
AACC treatment inflammation
ophthalmic steroid
AACC hyperosmotic
reduce vitreous volume
give if antisecretories and pilocarpine have no effect on IOP after 1 hour
PO glycerin or isosorbide 1-2g/kg
Iv mannitol 1.5-2g/kg
AACC
how to tell when crisis is improving?
IOP low, angle open, pupil miotic, check IOP q15-30 min, check angle when IOP drops to wnl
AACC at 1 hour after meds, IOP still high. tx?
hyperosmotic PRN high IOP
repeat doses of BB, a-ag, pilocarpine
may add ophthalmic steroid
