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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
GLC1E
Chromosome 10
26
GLC1F
Chromosome 7
27
Where is MYOC gene located?
Long (q) arm of chromosome 1 between positions 23 and 24
28
Screening for POAG
IOP measurements Optic disc evaluation Visual field testing
29
Glaucoma Suspects
Normal visual fields; open, normal angles + Elevated IOP and/or abnormal optic disc/nerve fiber layer
30
Gonioscopy
Examination to see whether the area where fluid drains out of your eye is open or closed
31
Pachymetry
Medical device used to measure the thickness of eye's cornea
32
Where is aqueous continuously produced?
By ciliary body on diurnal curve
33
What is the turnover of aqueous?
Every 1.5 to 3 hours
34
Aqueous flows...
from posterior chamber through pupil into anterior chamber
35
Where does aqueous filter?
Trabecular meshwork (90%) Ocular venous system (10%) ---Uveoscleral outflow
36
Pupil is controlled by...
Sympathetic dilates by contraction of dilator muscle Parasympathetic constricts by contracting sphincter muscle
37
Ciliary body is controlled by...
Sympathetic for aqueous production Parasympathetic causing ciliary body muscle movement
38
Treatment of Glaucoma
Decrease IOP by decreasing aqueous production or increasing outflow
39
Medications that decrease aqueous production
Beta Adrenergic Antagonists Systemic & Topical CA inhibitors
40
Medications that increase outflow
Prostaglandin Analogs Cholinergic Agonists Miotics: Parasympathetic Agents
41
Medications that decrease aqueous production and increase outflow
Adrenergic Agonists Osmotic Agents
42
most beta adrenergic antagonists are
nonselective
43
beta adrenergic antagonist mechanism of action
reduce the production of the aqueous humor
44
beta adrenergic antagonists dosing
very effective once to twice daily
45
side effects of beta adrenergic antagonists
worsening of asthma/emphysema, bradycardia, depression, confusion, worsening of myasthenia graves, low blood pressure, fatigue
46
betaxolol
betoptic more selective than the other BAA on the eye carries less risk of cardiac/pulmonary side effects
47
Timolol
timoptic non selective BAA - blocks both beta1 and beta 2 adrenergic receptors
48
timolol does not have significant
intrinsic sympathomimietic activity, local anesthetic or direct myocardial depressant activity
49
timolol, when applied topically in the eye
reduces IOP whether or not accompanied by glaucoma
50
B-adrenergic blocking agents reduce
cardiac output in BOTH healthy subjects and patients with heart diseases
51
Pharmacokinetics of Timolol
well absorbed, considerable 1st pass metabolism primarily excreted in urine half life in plasma - 4 hours
52
Prostaglandin analogs MOA
increase the outflow of fluid from the eye
53
Prostaglandin analogs dosing
once a day
54
side effects of prostaglandin analogs
change color of the iris thicken/darken eyelashes redness of the eyes inflammation inside the eye
55
examples of prostaglandin analogs
latanoprost - Xalatan Travoprost - Travatan Bimatoprost - Lumigan
56
Alpha Adrenergic Agonists MOA
reduce the production of aqueous humor and increase the outflow from the eye act like adrenaline
57
Most popular adrenergic agonist
Brimonidine - Alphagan
58
Brimonidine side effects
12% risk of significant local allergic reactions
59
alpha 2 agonists
epinephrine - epifrin dipivefrin - propine apraclonidine - lopidine brimonidine - alphagan-P brimonidine and beta blocker - Combigan
60
Cholinergic agonists MOA
increasing the outflow of fluid from the eye may lead to side effects if used frequently
61
short acting cholinergic agonists
Pilocarpine Carbachol
62
Long acting Cholinergic agonists
echothiophate iodide
63
side effects of cholinergic agonists
headache eyeache smaller pupils blurred/dim vision nearsightedness
64
Carbonic Anhydrase MOA
bidirectional conversion of CO2 and H2O into bicarbonate and protons play major roles in respiration, digestion and whole body/cellular pH regulation
65
carbonic anyhdrase inhibitors MOA
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
eyedrops forms of CAIs
dorzolamide - Truspot brinzolamide - Azopt
67
dosing of CAI eyedrops
2-3 times a day (8-12 h)
68
oral forms of CAIs
Acetazolamide - Diamox Methazolamide - Neptazane Dichlorophenamide - Daranide
69
reasons to use an oral CAI over a topical CAI
may be used to remove fluid from the body, including the eye
70
why are oral CAIs limited in use?
they reduce body potassium cause kidney stones numbness or tingling sensations in the arms and legs fatigue nausea
71
Possible side effects of carbonic anhydrase inhibitors
possible metallic taste frequent urination tingling in the fingers and toes
72
(CAIs) systemic adverse effects are unusual despite the
accumulation of drug in red blood cells
73
timolol 0.5%/ dorzolamide 2%
Cosopt dosed - bid produced equivalent IOP lowering to each product dosed separately
74
Nasolacrimal occlusion
improves the therapeutic index of anti glaucoma medications
75
what does a nasolacrimal occlusion prevent?
prevents the drug from flowing into the drainage duct more medicine in the eye --> drug is more effective
76
Dorzolamide MOA
Inhibition in ciliary processes slows formation of bicarbonate ions --> reduction in fluid and sodium transport --> lower IOP
77
Dorzolamide accumulates in
RBCs during chronic dosing as a result of binding to CAII
78
N-desethyl metabolite
inhibits CAII less potently than dorzolamide also inhibits CAI this metabolite also accumulates in RBCs when its binds to CAI
79
after dorzolamide is stopped, the slower elimination phase has a half life of
four months
80
parasympathomimitic agents MOA
increasing the aqueous outflow from the eye
81
parasympathomimetic agents
mitotics narrow the pupils opposes adrenaline like substances
82
side effects of parasympathomimetic agents
a small pupil, blurred vision, aching brow, increased risk of retinal detachment
83
why are prostaglandins agonists/ Beta blockers used over parasympathomimetic agents used?
because parasympathomimetic agents are used 3-4 times a day and the others are less
84
pilocarpine
used to keep pupil small in patients with plateau iris used in patients with a narrow angle prior to laser iridotomy
85
osmotic agents
treat sudden forms of glaucoma where the eye pressure remains extremely high despite other treatments
86
osmotic agents examples
isosorbide mannitol
87
isosorbide
Ismotic by mouth release pressure via vasodilation
88
mannitol
osmitrol IV release water content via diuresis
89
MOA of mannitol
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
MOA of isosorbide
vasodilators relaxing the blood vessel, heart doesn't work as hard, doesn't need as much oxygen

Pharmacology (18 decks)

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