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NMSP Exam 1 > Lecture 3: Ocular Pharm/Glaucoma > Flashcards

Lecture 3: Ocular Pharm/Glaucoma Flashcards

1
Q

List the 5 β-blocking drugs that are used in glaucoma?

A
  • Betaxolol
  • Timolol
  • Metipranolol
  • Levobunolol
  • Carteolol
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2
Q

What are the two α2-adrenergic agonists used in the treatment of glaucoma?

A
  • Apraclonidine
  • Brimonidine
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3
Q

What are the three prostaglandin analogs used in the treatment of glaucoma?

A
  • Latanoprost
  • Bimatoprost
  • Travoprost
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4
Q

What are the two topical carbonic anhydrase inhibitors used in the treatment of glaucoma?

A
  • Brinzolamide
  • Dorzolamide
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5
Q

What are the two systemic carbonic anhydrase inhibitors used in the treatment of glaucoma?

A
  • Acetazolamide
  • Methazolamide
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6
Q

What are the two muscarinic agonists used in the treatment of glaucoma?

A
  • Carbachol
  • Pilocarpine
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7
Q

What are the two cholinesterase inhibitors used in the treatment of glaucoma?

A
  • Demecarium
  • Echothiophate
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8
Q

Function of iris circular muscle and via which receptor?

A
  • Constricts pupil to cause miosis
  • Effect is due to activation of M3 receptor
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9
Q

Function of iris radial muscle and via which receptor?

A
  • Dilates pupil to cause mydriasis
  • Effect is due to activation of α1 adrenergic receptor
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10
Q

What is the function of the ciliary muscle of the eye and via which receptor?

A
  • Causes accomodation of the eye to near vision
  • Opens up trabecular meshwork, improving outflow of aqueous humor into canal of Shlemm, decreasing intraocular pressure
  • M3 receptors contract the muscle
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11
Q

Function of the ciliary epithelium of the eye and via which receptor?

A
  • Produces (secretes) aqueous humor
  • β receptor activation increases humor production
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12
Q

Activation of which sympathetic receptor will increase production of aqueous humor?

Which receptors will cause a decrease?

A
  • β-receptor activation will increase production
  • α-receptor activation will decrease production
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13
Q

Which muscles of the eye are involved in improving the outflow of aqueous humor; which receptor mediates this?

A
  • Contraction of ciliary musle - muscarinic receptor
  • Contraction of iris circular muscle - muscarinic receptor
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14
Q

What is the function of Prostaglandin F2α on aqueous humor flow?

A

Improves uveoscleral, or unconventional outflow

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15
Q

Contraction of the iris radial muscle (α1 receptor) has what effect on the outflow of aqueous humor?

A

Mydriasis —> decreased outflow (conventional outflow)

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16
Q

Increased ________ is though to play an important role in the pathogenesis of glaucoma

A

Intraocular pressure

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17
Q

Which anatomical changes may predispose someone to developing closed-angle glaucoma?

A
  • Shallow anterior chamber
  • Narrow angle between cornea and iris
  • Tight contact between iris and the lens
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18
Q

Current pharmacotherapy of glaucoma is directed at producing what effect?

A

Reduction of IOP

19
Q

What is the goal/target for reducing IOP when using pharmacotherapy for glaucoma?

A
  • Decrease IOP by 30%
  • Want to have IOP less than 21 mmHg
20
Q

How long should you wait between treatments when administering 2 separate agents for glaucoma?

A

10 mins

21
Q

How much time should be given in between treatments of glaucoma if you are wanting to change the type of drug being used?

A

One day overlap

22
Q

What are the 3 first line agents for the treatment of open angle glaucoma?

A
  • Prostaglandin analogues
  • β-blockers - timolol is favored
  • Brimonidine (α2-adrenergic agonist)
23
Q

What are the 3 second line agents for the treatment of open angle glaucoma?

A
  • Pilocarpine (muscarinic agonist)
  • Apraclonidine (α2-adrenergic agonist)
  • Topical carbonic anhydrase inhibitors
24
Q

What are the 3 agents used as a last line therapy for the treatment of open angle glaucoma?

A
  • Carbachol (muscarinic agonist)
  • Inhibitors of cholinesterase
  • Oral carbonic anhydrase inhibitors
25
Q

Why are β-blockers commonly used in the treatment of glaucoma?

A
  • Convenience of dosing
  • Relative lack of adverse effects
26
Q

Why is the β-blocker, timolol, favored for the treatment of glaucoma?

A
  • Lacks local anesthetic effects
  • Available as generic
  • Full antagonist
  • Shown to be as effective as pilocarpine
27
Q

What is the MOA of timolol in the treatment of glaucoma?

A

Reduces production of aqueous humor by the ciliary body by blocking β receptors

28
Q

Adverse local effects of β-blockers when treating glaucoma?

A
  • Stinging
  • Dry eyes
  • Blurred vision
  • Blepharitis, and (rarely) keratitis and conjunctivitis
29
Q

Adverse systemic effects of β-blockers when treating glaucoma (i.e., heart, airways, and metabolically)?

A
  • Heart: negative inotropic effect
  • Airways: bronchospasm
  • Hyperlipidemia
  • Exacerbation of hypoglycemia (in patients on insulin)
30
Q

Which drug-drug interaction must be considered when treating glaucoma with a β-blocker?

Increases risk for what?

A
  • May interact with orally given verapamil
  • Increases risk of cardiac depression and heart block
31
Q

β-blockers should be used with caution in patients with what underlying conditions?

A
  • Bradycardia
  • AV block
  • Heart failure
  • Atherosclerosis
  • Diabetes

*As well as receiving oral β-blocking therapy

32
Q

Of the prostaglandin analogs, which is the most effective at lowering IOP for treatment of glaucoma?

A

Bimatoprost

33
Q

What is the frequency and the route of administration for prostaglandin analogs in the treatment of glaucoma?

A

Given once daily at nighttime (1 drop daily)

34
Q

What are some of the benefits of using prostaglandin analogs in the treatment of glaucoma?

A
  • More efficiently reduce IOP than β-blockers
  • Systemic side effects are not significant
35
Q

What are 4 local side effects that may result from using prostaglandin analogs for the treatment of glaucoma?

Which effects are irreversible and which are reversible?

A
  • Corneal erosions
  • Conjunctival hyperemia
  • Iris hyperpigmentation (occurs after several months of therapy and is irreversible)
  • Hypertrichosis, hyperpigmentation around eye lashes and eyelids are reversible upon discontinuation of therapy
36
Q

Which α2-agonist is the first line agent for the treatment of glaucoma?

A

Brimonidine

37
Q

Why is the α2-agonist, Apraclonidine, not preferred for the treatment of glaucoma?

A

Frequent allergic reactions, development of tachyphylaxis

38
Q

What is the MOA of α2-agonists in tx of glaucoma?

A

Decrease the rate of aqueous humor production

39
Q

What are the adverse systemic and local effects of α2-agonists used in the treatment of glaucoma?

A
  • Systemic: dizziness, fatigue, dry mouth, bradycardia, reduced BP
  • Local: allergic reaction (eyelid edema, itching, hyperemia)
40
Q

What is the algorithm for pharmacotherapy of open angle glaucoma?

A
  • Start with β-blocker; if intolerance to specific β-blocker, use class alternative
  • β-blockers contraindicated, use alternative 1st line agent (prostaglandins or brimonidine)
  • If intolerance to prostaglandin agent, use class alternative
  • If contraindications to all 1st class agents, use topical carbonic anhydrase inhibitors (2nd-line)
  • If monotherapy fails, use a combination therapy
  • If intolerance or inadequate response to the combo therapy, use laser or a surgical procedure
41
Q

With closed angle glaucoma the goal is a rapid reduction of IOP, what drugs are used in preparation for surgery?

A
  • Systemic osmotic diuretics: IV Mannitol (1-2 g/kg)
  • Pilocarpine = drug of choise before surgery - induces miosis
42
Q

What occurs during surgery for a closed angle glaucoma?

A

Produce a hole in the iris facilitating the humor outflow (iridectomy)

43
Q

What 3 drugs are contraindicated with open angle glaucoma?

A
  1. Glucocorticoids (topical, systemic, nasal, inhaled)
  2. Fenoldopam
  3. Topic antimuscarinic drugs
44
Q

Which drugs are contraindicated with closed angle glaucoma due to their ability to cause mydriasis and possible angle closure?

A
  • Antimuscarinic drugs (topical, systemic)
  • Drugs w/ alpha-adrenomimetic activity (topical)
  • Tricyclic antidepressants and Serotonin-norepinephrine reuptake inhibitors (due to potent antimuscarinic action)

NMSP Exam 1 (18 decks)

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