Pharmacology Exam 3- Pharmacology Of The Eye

Front 1

4 layers of the eye from outermost to innermost

Back 1

cornea-->sclera
uveal tract (iris-->ciliary body-->choroid)
pigment epithelium

Front 2

describe 'consensual pupil response' and how what this is used to diagnose

Back 2

stimulation of retinal cells sends signals to the brain causing dilation or constriction of pupil, which are then processed to send the same signal to the other eye.

used to assess brain dmg

Front 3

dilator pupillae vs. constrictor pupillae muscles

Back 3

dilator pupillae = radial muscles (contract to dilate pupil)

constrictor pupillae muscle = sphincter muscle- contracts to constrict pupil

Front 4

3 stimulators of mydriasis and their relative strength (strong or weak)

Back 4

1) low light levels (strong dilation)
2) inhibition of parasympathetic branch via M3 receptor antagonists in iris (strong dilation)
3) stimulation of sympathetic branch via a1 agonists in iris (weak dilation)

Front 5

4 stimulators of miosis and their relative strength (strong or weak)

Back 5

1) high light levels (strong)
2) stimulation of M3 receptors in the iris (strong)
3) inhibition of sympathetic a1 receptors in iris (weak)
4) opioid receptors in CNS stimulation (pinhole pupil) --> quite strongq

Front 6

describe accommodation in the eye (what is it, what is the mechanism?)

Back 6

mechanism necessary to focus visual image on the retina

does so by altering the refractive power of the lens via ciliary muscles, attached to suspensory ligaments, attached to the lens. contraction of ciliary muscles (circular) relaxes suspensory ligaments and makes lens more spherical for close range focus (increase radius of curvature; near accommodation)

Front 7

what 2 interfaces does light refract through before reaching retina?

Back 7

cornea:air interface
lens

Front 8

what receptor agonists elicit contraction of ciliary muscle?

Back 8

muscarinic agonists

Front 9

describe what cycloplegia is, and how you might elicit it

Back 9

cycloplegia is essentially paralysis of the ciliary muscle (loss of accommodation).

you can achieve this by using muscarinic antagonists like atropine

Front 10

what would happen to accommodation reflex if you administered adrengeric agonists or antagonists to the eye?

Back 10

nothing. there are no adrengeric receptors on the ciliary muscle

Front 11

describe presbyobia. compare young vs. old refractory power.

Back 11

loss of accommodation due to lens becoming less flexible with age (can only accommodate 1-2 diopters at old age vs. 12 at young age)

Front 12

describe the production and flow of aqueous humor (3)

Back 12

1) secreted by blood vessels in the ciliary body
2) flows through pupil into anterior chamber
3) drains

Front 13

2 modes of drainage for aq. humor

Back 13

1) trabelcular meshwork-->canal of schemm-->episcleral veins
2) uveoscleral drainage (not as dependent on IOP)

Front 14

3 targets for the affecting of aq. humor production

Back 14

alpha adrenoreceptors
beta receptors
carbonic anhydrase (affects osmolarity of the eye)

Front 15

a1/a2 receptors and their effects (if stimulated) on aq. humor production

Back 15

a1- decrease aq humor production by constricting blood vessels-->decrease blood flow through ciliary body
a2- stimulation of ciliary body (decrease aq humor)

Front 16

b1 adrenoreceptor and effects on aq humor production (if stimulated)

Back 16

stimulates ciliary body to increase aq humor (ergo use beta21 blockers)

Front 17

carbonic anhydrase and effects on aq humor

Back 17

carbonic anhydrase produces HCO3-. active transport of HCO3- and Na+ is required for aqueous humor production (so inhibiting it would decrease production)

Front 18

desired properties of ophthalmic drug (structure)

Back 18

must be lipophilic and uncharged (to cross corneal membrane)

Front 19

effect of eye color on opth. drugs

Back 19

melanin in iris can bind some drugs like atropine. therefore in people with dark eyes, this can cause drugs to have longer onsets and longer durations (possible overdose)

Front 20

local admin of drug to eye- why is this preferable to systemic in terms of adverse rxns?

Back 20

systemic adverse rxns risks are decreased (but not eliminated)

Front 21

muscarinic antagonists and their usage in the eye (specify receptor). purpose?

Back 21

used to block M3 receptors in the iris (and ciliary muscle) to elicit mydriasis (and cycloplegia)

dilation of pupil can allow better viewing of the fundus (interior surface of the eye)

Front 22

longest lasting antimuscarinic

Back 22

atropine (7-10 days)

Front 23

shortest lasting antimuscarinic

Back 23

tropicamide (0.25 days)

Front 24

mid range duration antimuscarinics (3)

Back 24

scopolamine (3-7 days)
homatropine (1-3)
cyclopentolate (1)

Front 25

what if you do not want to elicit cycloplegia in a pt, but still want to dilate pupils?

Back 25

use adrenergic receptor agonist

Front 26

glaucoma open vs. closed angle treatment options

Back 26

closed angle = surgery or drugs

open angle = drugs

Front 27

glaucoma- definition and cause

Back 27

elevation of IOP > 21 mm HG due to inadequate drainage of aq. humor

Front 28

IOP definition

Back 28

equilibrium state of pressure in eye determined by the rate of aq. humor production vs. drainage rate

Front 29

2 goals of drugs used to treat glaucoma

Back 29

1) decrease aq. humor production 2) increase drainage of aq. humor

Front 30

what happens if glaucoma goes untreated? (2)

Back 30

optic nerve dmg/visual field changes

Front 31

what is open vs. closed angle glaucoma? (what's the difference? what is the angle being referred to?)

Back 31

refers to filtration angle formed between cornea and iris. in open angle glaucoma the issue is not the angle of filtration, but rather "clogged pipes".

pressure can push iris flap close to cornea which blocks drainage of aq. humor

additionally open angle is chronic, whereas closed angle is acute.

Front 32

cause of open angle glaucoma

Back 32

primary defect of inadequate drainage into canal of schlemm

Front 33

4 categories of drug for treating open angle glaucoma

Back 33

1) beta 1 receptor antagonists
2) a2/a1 receptor agonist
3) carbonic anhydrase inhibitor (diuretic? decreases production)
4) muscarinic agonists (M3) - MAY improve uveoscleral outflow

Front 34

timolol vs. betaxalol= why would you use betaxalol over timolol

Back 34

betaxalol is b1 selective antagonist, meaning it won't cause bronchoconstriction in pt with asthma or copd

Front 35

-olol (timolol, carteolol, levobunolol, metipranolol)

Back 35

beta 1/2 antagonists for open angle glaucoma

Front 36

dipivefrin (2)

Back 36

alpha agonist used for open angle glaucoma

prodrug metabolized to epi

Front 37

epinephrine in treatment of glaucoma

Back 37

for open angle glaucoma
alpha agonist- constrict vessels and decrease ciliary body production of aq. humor

Front 38

apraclonidine (compare when you would use it to epi/dipivefrin)

Back 38

alpha agonist used for open angle glaucoma

used for extreme/acute cases only

Front 39

carbachol, pilocarpine

Back 39

muscarinic agonists (M3) for treating open angle glaucoma- can maybe increase uveoscleral drainage

Front 40

close angle glaucoma definition

Back 40

peripheral iris balloons out towards cornea and blocks drainage of aq humor

Front 41

2 acute treatments (temporary relief) for closed angle glaucoma

Back 41

1) systemic- mannitol/glycerol- increases blood osmolarity to decrease filtration (decrease aq humor)
2) topical- miotics like carbachol/pilocarpine (M3 receptor agonists that contract and tighten iris)

Front 42

cure for closed angle glaucoma

Back 42

YAG laser to create a small hole in iris (iridectomy)

Front 43

precautions when treating closed angle glaucoma

Back 43

do not use drugs that dilate the pupil (mydriatics)- for example to examine the eye further

pupil dilation/cycloplegia can exacerbate closed angle glaucoma and decrease drainage even further