Toxic responses of the eye Flashcards
main areas of ocular drug metabolism
cornea and retina
rich in enzymes more susceptible
cornea susceptibility
avascular so less
lens susceptibility
avascular not very susceptible
phenothiazines (chlorpromazine) toxicity
pigmentation ranging from white to yellow to tan
begins of the anterior surface of the lense . cornea becomes involved when lenticular pigmentation reaches grade 3
dose of chlorpromazine toxic
total cumulative >2500g
how often should ppl on chlorpromazine get thier eyes checked
on high doses or long term low doses should be annually
mechanism of corticosteroid toxicity
altered lens epithelium electrolyte balance
binding to proteins of the lens (corticosteroid crystalling adducts )
all forms!
corticosteroid toxicity unlikely in
<10mg prednisone or treated for less than a year
how often should ppl on steroids get thier eyes check
long term oral steroids every 6 months
is corticosteroid toxicity reversible
yes
why is an eye exam recommended at baseline and every 6 months with quetiapine
cataract development has been observed
normal intraocular pressure
10-22mmhg
open angle glaucoma
absence of pain
slow loss of peripheral visual field
often unnoticed
closed angle glaucoma
happens to indiiduals genetically susceptible
narrow anterior chamber angle
caused by anything that dilates the pupil
painful
aqueous humor flow
flows between the posterior surface of the iris and the anterior lens surface
corticosteroids effect on pressure
increased ressitance to aqueous humor outflow seen with topical opthalmic agents
agents affecting IOP
prolonged continuouis use of beclomethasone or budesonide daily for >3month
phenothiazines
TCA
how are tears secreted
from lachrymal gland stimulated by cholinergic and adrenergic nerves
drugs increasing production of tears
cholinergic - pilocarpine
adrenergic agonist - ephedrine
drugs causing orange colored tears
oral erythromycin and rifampin
what is anterior uveitis
inflammation of uvea (iris, ciliary body, choroid)
symptoms of anterior uveitis
eye pain
conjuctival redness
photophobia and blurred vision
pupil is small and respond sluggishly to light
drugs associated with vueitis
rifabutin
bisphosphonates
retina susceptibility
highly organized structure wiht porrly developed repair
vascularized
very sensitive
damage can lead to permanent damage
drugs affecting retina
chloroquine and hydroxychloroquine digoxin indomethacin tamoxifen retinoids quinine
is chloroquine/hydroxy retinopathy reversible
no
safe dose of hydroxychloroquine
<400mg/day
visual symptoms of digoxin toxicity
dychromatopsia (color blindness) flickering or flasing light colored spots surround by coronas snowy hazy or vblurred vision glare sensitivity can occur at therapeutic doses
digoxin mechanism of toxicity
inhibit nakATPase
cone receptor function
is digoxin toxicity reversible
within a few weeks after dose reduction or discontinuation
indomethacin dose producing toxicity
chronic 50-200mg/day for 1-2yrs
symptoms of indomethacin toxicity
corneal opacities paramacular depigmentation decreased visual acuity altered visual fields blue yellow color deficity increased threshold for ark adaptation
is indomethacin toxicity reversible
color disturbances return to normal after discontinuation
tamoxifen xicity odse
chornic high dose
180mg/day for 3 year
mechanism of tamoxifen toxicity
permanent decrease in visual acuity and abnormal visual fields
crystallizes in the retina
retinoids toxicity symptoms
poor night vision
glare sensitivity
problems with color detection
retinoids mechanism of toxicity
inhibition of retinol dehydrogenas which impairs rod cell function
quinine symptoms of toxicity
blurred vision
central and peripheral scotomata (blind spot)
complete blindness
when does vision loss ccur with quinine
can occur as late as 14hr after OD
mechanism of quinine toxicity
neurotoxic injury to retinal ganglion cells permamne t loss and optic nerve
retinal vasoconstiction
drugs affecting optical nerve
ethambutol
ethambutol toxicity
decreased contrast sensitivity an color vision
signs of optical neuropathy caused by ethambutol
central scotoma
visual field loss
decreased visual activity
dose of ethambutol toxicity
25-50mg/kg/d may cause loss of vision in 1-7months
is ethambutol vision loss reversable
yes
how to eliminate visual toxicity with ethambutol
biweekly high doses
what is alcohol tobacco amblyopia
lazy eye due to combo of alcohol tobacco and nutrional deficiency
cholinergic action of eye
cholinergic innervation of the iris sphincter aka the constrictor by cranial nerve
symphathetic action on eye
innervation of the radial muscle of the iris aka the dilator
miosis =
constriction
mydriasis =
dilation
drugs causing miosis
cholinergic agent
opiates
phenothiazine
sedative hypnotic
drugs causing mydriasis
anticholinergic
antidepressant
sympathomimetics
what is nystagmus
unvoluntary eye movement
what causes jerk nystagmus
phenytoin
what causes vertical nystagmus
rare usually structural lesion of cns
pehncyclidine
ketamine
DM
nystagmus and opthalmoplegia (paralysis) caused by
thiamine deficiency
drug abuse ocular complications
quinine amblyopia (lazy eye) if found in heroin
talc retinopathy
infectious complications
HIV related
cocaine diffus vasospasm - retinal ischemia and blindness
crack eye - corneal injury from the smoke numbing sensation
