Pharmacology of the Eye

Question 1

Phase I metabolism

Answer 1

Hydrolysis, oxidation, reduction

Question 2

Phase II metabolism

Answer 2

Conjugation (methylation, etc)

Question 3

Absorption of drugs in eye determined by?

Answer 3

Length of time drug stays in the inferior fornix and precorneal tear film

Question 4

How to ocular drugs enter systemic circulation?

Answer 4

Via the nasal mucosa

Question 5

How do ocular drugs get to interior ocular structures?

Answer 5

Via aqueous humor by trabecular meshwork.

Question 6

Metabolism?

Answer 6

tear and tissue proteins, diffusion. Hepatic if enters systemically

Question 7

Does first pass metabolism occur if absorbed by nasal mucosa?

Answer 7

No.

Question 8

Pupillary constriction

Answer 8

Parasympathetic inputs contract circular muscle (miosis)

Question 9

Pupillary dilation

Answer 9

Sympathetic stimulation of radial muscles (mydriasis)

Question 10

Ciliary body consists of

Answer 10

Ciliary muscle and ciliary epithelium

Question 11

Parasympathetic stimulation to ciliary muscle

Answer 11

Causes contraction, accommodation (near focus), zonule fibers relax

Question 12

Cyclospasm

Answer 12

Severe ciliary muscle contraction. Can be caused by AChE inhibitors

Question 13

Cycloplegia

Answer 13

Block of accommodation by cholinergic antagonists

Question 14

Effect of parasympathetic stimulation on trabecular meshwork?

Answer 14

Tension opens pores and facilitates outflow of aqueous humor into canal of Schlemm. This decreases interocular pressure

Question 15

Where does drainage from canal of schlemm go?

Answer 15

Into superchoroidal space

Question 16

Effect of sympathetic stimulation on aqueous humor secretion?

Answer 16

Promotes secretion by stimulating beta receptors.

Question 17

Predominant beta receptor in eye?

Answer 17

B2

Question 18

Predominant beta receptor in heart?

Answer 18

B1

Question 19

Predominant beta receptor in lungs?

Answer 19

B2

Question 20

How to treat open-angle glaucoma?

Answer 20

Decrease production of aqueous humor, increase outflow at canal of schlemm or in sclera

Question 21

Latanoprost

Answer 21

Prostaglandin agonist which is 1st line for glaucoma. Works by increasing aqueous humor outflow via uveoscleral pathway. Unclear how

Question 22

Creation of prostaglandins

Answer 22

From arachidonic acid (usually in membranes), COX oxygenizes to create prostaglandins, thromboxane, and prostacyclin

Question 23

Effect of prostaglandins

Answer 23

Targets all over body including smooth muscle and eye

Question 24

Prostaglandin agonist side effects

Answer 24

Blurred vision, burning sensation in eye, punctate keratopathy (keratitis)

Question 25

Punctate keratopathy

Answer 25

Cornification of cornea thought to be due to irritation from prostaglandin agonists or from a preservative.

Question 26

Timolol

Answer 26

B1 and B2 antagonist, second line for glaucoma. Prevents creation of aqueous humor by ciliary epithelium

Question 27

Mechanism of action of B receptor mediated creation of aqueous humor

Answer 27

Linked to Gs, so produces cAMP, which is thought to increase aqueous humor.

Question 28

Side effects of B antagonists

Answer 28

Blurred vision, burning sensation in eye, dry eyes, cough, bradycardia, hypotension. Systemic side effects unlikely.

Question 29

Why do beta blockers cause hypotension?

Answer 29

Because they slow heart rate, which decreases CO, which decreases MAP.

Question 30

Brimonidine

Answer 30

Alpha2 agonist. This works in 2 ways. 1) Binding to presynaptic A2 receptor, which decreases the amount of NE in synapse. 2) Binding to postsynaptic A2 receptor (Gi) decreasing cAMP and preventing aqueous humor production

Question 31

How does brimonidine cause hypotension

Answer 31

Because it works more strongly at the autoreceptor in vascular musculature, which prevents alpha mediated constriction.

Question 32

Dorzolamide

Answer 32

Carbonic anhydrase inhibitor. Works by preventing secretion of HCO3 into aqueous humor.

Question 33

Carbachol/pilocarpine

Answer 33

Cholinergic agonists, these cause muscarinic induced ciliary muscle contraction, increasing outflow at trabecular mesh.