Toxic responses of the eye Flashcards

(58 cards)

1
Q

main areas of ocular drug metabolism

A

cornea and retina

rich in enzymes more susceptible

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2
Q

cornea susceptibility

A

avascular so less

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3
Q

lens susceptibility

A

avascular not very susceptible

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4
Q

phenothiazines (chlorpromazine) toxicity

A

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

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5
Q

dose of chlorpromazine toxic

A

total cumulative >2500g

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6
Q

how often should ppl on chlorpromazine get thier eyes checked

A

on high doses or long term low doses should be annually

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7
Q

mechanism of corticosteroid toxicity

A

altered lens epithelium electrolyte balance
binding to proteins of the lens (corticosteroid crystalling adducts )
all forms!

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8
Q

corticosteroid toxicity unlikely in

A

<10mg prednisone or treated for less than a year

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9
Q

how often should ppl on steroids get thier eyes check

A

long term oral steroids every 6 months

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10
Q

is corticosteroid toxicity reversible

A

yes

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11
Q

why is an eye exam recommended at baseline and every 6 months with quetiapine

A

cataract development has been observed

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12
Q

normal intraocular pressure

A

10-22mmhg

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13
Q

open angle glaucoma

A

absence of pain
slow loss of peripheral visual field
often unnoticed

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14
Q

closed angle glaucoma

A

happens to indiiduals genetically susceptible
narrow anterior chamber angle
caused by anything that dilates the pupil
painful

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15
Q

aqueous humor flow

A

flows between the posterior surface of the iris and the anterior lens surface

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16
Q

corticosteroids effect on pressure

A

increased ressitance to aqueous humor outflow seen with topical opthalmic agents

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17
Q

agents affecting IOP

A

prolonged continuouis use of beclomethasone or budesonide daily for >3month
phenothiazines
TCA

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18
Q

how are tears secreted

A

from lachrymal gland stimulated by cholinergic and adrenergic nerves

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19
Q

drugs increasing production of tears

A

cholinergic - pilocarpine

adrenergic agonist - ephedrine

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20
Q

drugs causing orange colored tears

A

oral erythromycin and rifampin

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21
Q

what is anterior uveitis

A

inflammation of uvea (iris, ciliary body, choroid)

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22
Q

symptoms of anterior uveitis

A

eye pain
conjuctival redness
photophobia and blurred vision
pupil is small and respond sluggishly to light

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23
Q

drugs associated with vueitis

A

rifabutin

bisphosphonates

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24
Q

retina susceptibility

A

highly organized structure wiht porrly developed repair
vascularized
very sensitive
damage can lead to permanent damage

25
drugs affecting retina
``` chloroquine and hydroxychloroquine digoxin indomethacin tamoxifen retinoids quinine ```
26
is chloroquine/hydroxy retinopathy reversible
no
27
safe dose of hydroxychloroquine
<400mg/day
28
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 ```
29
digoxin mechanism of toxicity
inhibit nakATPase | cone receptor function
30
is digoxin toxicity reversible
within a few weeks after dose reduction or discontinuation
31
indomethacin dose producing toxicity
chronic 50-200mg/day for 1-2yrs
32
symptoms of indomethacin toxicity
``` corneal opacities paramacular depigmentation decreased visual acuity altered visual fields blue yellow color deficity increased threshold for ark adaptation ```
33
is indomethacin toxicity reversible
color disturbances return to normal after discontinuation
34
tamoxifen xicity odse
chornic high dose | 180mg/day for 3 year
35
mechanism of tamoxifen toxicity
permanent decrease in visual acuity and abnormal visual fields crystallizes in the retina
36
retinoids toxicity symptoms
poor night vision glare sensitivity problems with color detection
37
retinoids mechanism of toxicity
inhibition of retinol dehydrogenas which impairs rod cell function
38
quinine symptoms of toxicity
blurred vision central and peripheral scotomata (blind spot) complete blindness
39
when does vision loss ccur with quinine
can occur as late as 14hr after OD
40
mechanism of quinine toxicity
neurotoxic injury to retinal ganglion cells permamne t loss and optic nerve retinal vasoconstiction
41
drugs affecting optical nerve
ethambutol
42
ethambutol toxicity
decreased contrast sensitivity an color vision
43
signs of optical neuropathy caused by ethambutol
central scotoma visual field loss decreased visual activity
44
dose of ethambutol toxicity
25-50mg/kg/d may cause loss of vision in 1-7months
45
is ethambutol vision loss reversable
yes
46
how to eliminate visual toxicity with ethambutol
biweekly high doses
47
what is alcohol tobacco amblyopia
lazy eye due to combo of alcohol tobacco and nutrional deficiency
48
cholinergic action of eye
cholinergic innervation of the iris sphincter aka the constrictor by cranial nerve
49
symphathetic action on eye
innervation of the radial muscle of the iris aka the dilator
50
miosis =
constriction
51
mydriasis =
dilation
52
drugs causing miosis
cholinergic agent opiates phenothiazine sedative hypnotic
53
drugs causing mydriasis
anticholinergic antidepressant sympathomimetics
54
what is nystagmus
unvoluntary eye movement
55
what causes jerk nystagmus
phenytoin
56
what causes vertical nystagmus
rare usually structural lesion of cns pehncyclidine ketamine DM
57
nystagmus and opthalmoplegia (paralysis) caused by
thiamine deficiency
58
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