Toxic responses of the eye Flashcards

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
Q

drugs affecting retina

A
chloroquine and hydroxychloroquine 
digoxin 
indomethacin 
tamoxifen 
retinoids 
quinine
26
Q

is chloroquine/hydroxy retinopathy reversible

A

no

27
Q

safe dose of hydroxychloroquine

A

<400mg/day

28
Q

visual symptoms of digoxin toxicity

A
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
Q

digoxin mechanism of toxicity

A

inhibit nakATPase

cone receptor function

30
Q

is digoxin toxicity reversible

A

within a few weeks after dose reduction or discontinuation

31
Q

indomethacin dose producing toxicity

A

chronic 50-200mg/day for 1-2yrs

32
Q

symptoms of indomethacin toxicity

A
corneal opacities
paramacular depigmentation
decreased visual acuity 
altered visual fields 
blue yellow color deficity
increased threshold for ark adaptation
33
Q

is indomethacin toxicity reversible

A

color disturbances return to normal after discontinuation

34
Q

tamoxifen xicity odse

A

chornic high dose

180mg/day for 3 year

35
Q

mechanism of tamoxifen toxicity

A

permanent decrease in visual acuity and abnormal visual fields
crystallizes in the retina

36
Q

retinoids toxicity symptoms

A

poor night vision
glare sensitivity
problems with color detection

37
Q

retinoids mechanism of toxicity

A

inhibition of retinol dehydrogenas which impairs rod cell function

38
Q

quinine symptoms of toxicity

A

blurred vision
central and peripheral scotomata (blind spot)
complete blindness

39
Q

when does vision loss ccur with quinine

A

can occur as late as 14hr after OD

40
Q

mechanism of quinine toxicity

A

neurotoxic injury to retinal ganglion cells permamne t loss and optic nerve
retinal vasoconstiction

41
Q

drugs affecting optical nerve

A

ethambutol

42
Q

ethambutol toxicity

A

decreased contrast sensitivity an color vision

43
Q

signs of optical neuropathy caused by ethambutol

A

central scotoma
visual field loss
decreased visual activity

44
Q

dose of ethambutol toxicity

A

25-50mg/kg/d may cause loss of vision in 1-7months

45
Q

is ethambutol vision loss reversable

A

yes

46
Q

how to eliminate visual toxicity with ethambutol

A

biweekly high doses

47
Q

what is alcohol tobacco amblyopia

A

lazy eye due to combo of alcohol tobacco and nutrional deficiency

48
Q

cholinergic action of eye

A

cholinergic innervation of the iris sphincter aka the constrictor by cranial nerve

49
Q

symphathetic action on eye

A

innervation of the radial muscle of the iris aka the dilator

50
Q

miosis =

A

constriction

51
Q

mydriasis =

A

dilation

52
Q

drugs causing miosis

A

cholinergic agent
opiates
phenothiazine
sedative hypnotic

53
Q

drugs causing mydriasis

A

anticholinergic
antidepressant
sympathomimetics

54
Q

what is nystagmus

A

unvoluntary eye movement

55
Q

what causes jerk nystagmus

A

phenytoin

56
Q

what causes vertical nystagmus

A

rare usually structural lesion of cns
pehncyclidine
ketamine
DM

57
Q

nystagmus and opthalmoplegia (paralysis) caused by

A

thiamine deficiency

58
Q

drug abuse ocular complications

A

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