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Pharmacology > Eye Disorders (Exam 2) > Flashcards

Eye Disorders (Exam 2) Flashcards

1
Q

Leading cause of blindness in US?

A

Age-related eye diseases

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2
Q

Amblyopia

A

Lazy eye

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3
Q

Strabismus

A

Imbalance of positioning of eyes

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4
Q

Glaucoma

A

Group of diseases that damage optic nerve and can result in vision loss and blindness

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5
Q

Glaucoma Progression

A

Ganglion cell death –> retinal nerve fiber layer change –> Optic nerve head changes –> Visual field changes

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6
Q

Primary Open-Angle Glaucoma (POAG)

A

Most common
Bilateral not always symmetric
Adult onset
Open, normal-appearing anterior chamber angles
Absence of secondary causes

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7
Q

Where do most medications of the eye act on?

A

Ciliary body and muscles

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8
Q

Open-Angle Glaucoma (OAG)

A

Intraocular pressure builds due to damage/blockage of drainage system in eye (trabecular meshwork)

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9
Q

Normal anatomy of the eye

A

Fluid flows freely through anterior chamber and exits through trabecular meshwork

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10
Q

What does open-angle mean?

A

Angle where iris meets cornea is wide and open

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11
Q

Angle-Closure Glaucoma

A

Less common
Blocked drainage canals leads to increased IOP (intraocular pressure)
Closed/narrow angle between iris and cornea

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12
Q

Types of eye drops to lower eye pressure

A

PROSTAGLANDINS
Rho kinase inhibitor
Nitric oxides
Miotic-cholinergic agents
Alpha-adrenergic agonists
Beta blockers
Carbonic anhydrase inhibitors

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13
Q

At risk population for Glaucoma

A

Elderly, african-americans, elevated IOP, relatives with glaucoma
Hyperopia (farsightedness)
High myopia (shortsightedness)

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14
Q

Which type of glaucoma doesn’t cause symptoms?

A

Open-Angle Glaucoma

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15
Q

Signs of Open-Angle Glaucoma

A

Gradual loss of peripheral vision
Tunnel vision is advanced stages

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16
Q

Signs of Angle-Closure Glaucoma

A

Develops suddenly
Sensitivity to light, cloudy eyes, halos around lights

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17
Q

Childhood Glaucoma

A

Asymptomatic in early stages
Congenital glaucoma
Total optic nerve atrophy and blindness

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18
Q

Causes of Secondary Glaucoma

A

Ocular vascular occlusion
Trauma, Uveitis, steroids, diabetes

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19
Q

High IOP correlates poorly with…

A

Presence of optic nerve damage

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20
Q

IOP level is related to…

A

POAG prevalence

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21
Q

MYOC or TIGR gene (GLC1A)

A

Chromosome 1

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22
Q

GLC1B

A

Chromosome 2

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23
Q

GLC1C

A

Chromosome 3

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24
Q

GLC1D

A

Chromosome 8

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25
Q

GLC1E

A

Chromosome 10

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26
Q

GLC1F

A

Chromosome 7

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27
Q

Where is MYOC gene located?

A

Long (q) arm of chromosome 1 between positions 23 and 24

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28
Q

Screening for POAG

A

IOP measurements
Optic disc evaluation
Visual field testing

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29
Q

Glaucoma Suspects

A

Normal visual fields; open, normal angles
+
Elevated IOP and/or abnormal optic disc/nerve fiber layer

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30
Q

Gonioscopy

A

Examination to see whether the area where fluid drains out of your eye is open or closed

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31
Q

Pachymetry

A

Medical device used to measure the thickness of eye’s cornea

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32
Q

Where is aqueous continuously produced?

A

By ciliary body on diurnal curve

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33
Q

What is the turnover of aqueous?

A

Every 1.5 to 3 hours

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34
Q

Aqueous flows…

A

from posterior chamber through pupil into anterior chamber

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35
Q

Where does aqueous filter?

A

Trabecular meshwork (90%)
Ocular venous system (10%)
—Uveoscleral outflow

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36
Q

Pupil is controlled by…

A

Sympathetic dilates by contraction of dilator muscle
Parasympathetic constricts by contracting sphincter muscle

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37
Q

Ciliary body is controlled by…

A

Sympathetic for aqueous production
Parasympathetic causing ciliary body muscle movement

38
Q

Treatment of Glaucoma

A

Decrease IOP by decreasing aqueous production or increasing outflow

39
Q

Medications that decrease aqueous production

A

Beta Adrenergic Antagonists
Systemic & Topical CA inhibitors

40
Q

Medications that increase outflow

A

Prostaglandin Analogs
Cholinergic Agonists
Miotics: Parasympathetic Agents

41
Q

Medications that decrease aqueous production and increase outflow

A

Adrenergic Agonists
Osmotic Agents

42
Q

most beta adrenergic antagonists are

A

nonselective

43
Q

beta adrenergic antagonist mechanism of action

A

reduce the production of the aqueous humor

44
Q

beta adrenergic antagonists dosing

A

very effective
once to twice daily

45
Q

side effects of beta adrenergic antagonists

A

worsening of asthma/emphysema, bradycardia, depression, confusion, worsening of myasthenia graves, low blood pressure, fatigue

46
Q

betaxolol

A

betoptic
more selective than the other BAA on the eye
carries less risk of cardiac/pulmonary side effects

47
Q

Timolol

A

timoptic
non selective BAA - blocks both beta1 and beta 2 adrenergic receptors

48
Q

timolol does not have significant

A

intrinsic sympathomimietic activity, local anesthetic or direct myocardial depressant activity

49
Q

timolol, when applied topically in the eye

A

reduces IOP whether or not accompanied by glaucoma

50
Q

B-adrenergic blocking agents reduce

A

cardiac output in BOTH healthy subjects and patients with heart diseases

51
Q

Pharmacokinetics of Timolol

A

well absorbed, considerable 1st pass metabolism
primarily excreted in urine
half life in plasma - 4 hours

52
Q

Prostaglandin analogs MOA

A

increase the outflow of fluid from the eye

53
Q

Prostaglandin analogs dosing

A

once a day

54
Q

side effects of prostaglandin analogs

A

change color of the iris
thicken/darken eyelashes
redness of the eyes
inflammation inside the eye

55
Q

examples of prostaglandin analogs

A

latanoprost - Xalatan
Travoprost - Travatan
Bimatoprost - Lumigan

56
Q

Alpha Adrenergic Agonists MOA

A

reduce the production of aqueous humor and increase the outflow from the eye
act like adrenaline

57
Q

Most popular adrenergic agonist

A

Brimonidine - Alphagan

58
Q

Brimonidine side effects

A

12% risk of significant local allergic reactions

59
Q

alpha 2 agonists

A

epinephrine - epifrin
dipivefrin - propine
apraclonidine - lopidine
brimonidine - alphagan-P
brimonidine and beta blocker - Combigan

60
Q

Cholinergic agonists MOA

A

increasing the outflow of fluid from the eye
may lead to side effects if used frequently

61
Q

short acting cholinergic agonists

A

Pilocarpine
Carbachol

62
Q

Long acting Cholinergic agonists

A

echothiophate iodide

63
Q

side effects of cholinergic agonists

A

headache
eyeache
smaller pupils
blurred/dim vision
nearsightedness

64
Q

Carbonic Anhydrase MOA

A

bidirectional conversion of CO2 and H2O into bicarbonate and protons
play major roles in respiration, digestion and whole body/cellular pH regulation

65
Q

carbonic anyhdrase inhibitors MOA

A

reduce IOP by decreasing ciliary body aqueous humor secretion
block active secretion of sodium and bicarbonate ions from the ciliary body to the aqueous

66
Q

eyedrops forms of CAIs

A

dorzolamide - Truspot
brinzolamide - Azopt

67
Q

dosing of CAI eyedrops

A

2-3 times a day (8-12 h)

68
Q

oral forms of CAIs

A

Acetazolamide - Diamox
Methazolamide - Neptazane
Dichlorophenamide - Daranide

69
Q

reasons to use an oral CAI over a topical CAI

A

may be used to remove fluid from the body, including the eye

70
Q

why are oral CAIs limited in use?

A

they reduce body potassium
cause kidney stones
numbness or tingling sensations in the arms and legs
fatigue
nausea

71
Q

Possible side effects of carbonic anhydrase inhibitors

A

possible metallic taste
frequent urination
tingling in the fingers and toes

72
Q

(CAIs) systemic adverse effects are unusual despite the

A

accumulation of drug in red blood cells

73
Q

timolol 0.5%/ dorzolamide 2%

A

Cosopt
dosed - bid
produced equivalent IOP lowering to each product dosed separately

74
Q

Nasolacrimal occlusion

A

improves the therapeutic index of anti glaucoma medications

75
Q

what does a nasolacrimal occlusion prevent?

A

prevents the drug from flowing into the drainage duct
more medicine in the eye –> drug is more effective

76
Q

Dorzolamide MOA

A

Inhibition in ciliary processes
slows formation of bicarbonate ions –> reduction in fluid and sodium transport –> lower IOP

77
Q

Dorzolamide accumulates in

A

RBCs during chronic dosing as a result of binding to CAII

78
Q

N-desethyl metabolite

A

inhibits CAII less potently than dorzolamide
also inhibits CAI
this metabolite also accumulates in RBCs when its binds to CAI

79
Q

after dorzolamide is stopped, the slower elimination phase has a half life of

A

four months

80
Q

parasympathomimitic agents MOA

A

increasing the aqueous outflow from the eye

81
Q

parasympathomimetic agents

A

mitotics
narrow the pupils
opposes adrenaline like substances

82
Q

side effects of parasympathomimetic agents

A

a small pupil, blurred vision, aching brow, increased risk of retinal detachment

83
Q

why are prostaglandins agonists/ Beta blockers used over parasympathomimetic agents used?

A

because parasympathomimetic agents are used 3-4 times a day and the others are less

84
Q

pilocarpine

A

used to keep pupil small in patients with plateau iris
used in patients with a narrow angle prior to laser iridotomy

85
Q

osmotic agents

A

treat sudden forms of glaucoma where the eye pressure remains extremely high despite other treatments

86
Q

osmotic agents examples

A

isosorbide
mannitol

87
Q

isosorbide

A

Ismotic
by mouth
release pressure via vasodilation

88
Q

mannitol

A

osmitrol
IV
release water content via diuresis

89
Q

MOA of mannitol

A

in the intravascular space increases the tonicity of the blood plasma
draws water out into intravascular space
once here, the mannitol is excreted in kidneys

90
Q

MOA of isosorbide

A

vasodilators
relaxing the blood vessel, heart doesn’t work as hard, doesn’t need as much oxygen

Pharmacology (16 decks)

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