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Ahmed Neuro 2 Depression > 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?

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
Why are β-blockers commonly used in the treatment of glaucoma?
- Convenience of dosing - Relative lack of adverse effects
26
Why is the β-blocker, **timolol**, favored for the treatment of glaucoma?
- **Lacks** local anesthetic effects - Available as generic - **Full antagonist** - Shown to be as effective as pilocarpine
27
What is the MOA of timolol in the treatment of glaucoma?
**Reduces** production of **aqueous humor** by the **ciliary body** by blocking β receptors
28
Adverse **local** effects of β-blockers when treating glaucoma?
- Stinging - Dry eyes - Blurred vision - Blepharitis, and (rarely) keratitis and conjunctivitis
29
Adverse **systemic** effects of β-blockers when treating glaucoma (i.e., heart, airways, and metabolically)?
- **Heart:** negative inotropic effect - **Airways:** bronchospasm - Hyperlipidemia - Exacerbation of hypoglycemia (in patients on insulin)
30
Which drug-drug interaction must be considered when treating glaucoma with a β-blocker? Increases risk for what?
- May interact with **orally** given **verapamil** - Increases risk of **cardiac depression** and **heart block**
31
β-blockers should be used with caution in patients with what underlying conditions?
- Bradycardia - AV block - Heart failure - Atherosclerosis - Diabetes \*As well as receiving oral β-blocking therapy
32
Of the prostaglandin analogs, which is the most effective at lowering IOP for treatment of glaucoma?
Bimatoprost
33
What is the frequency and the route of administration for prostaglandin analogs in the treatment of glaucoma?
Given **once** daily at nighttime (**1 drop daily**)
34
What are some of the benefits of using prostaglandin analogs in the treatment of glaucoma?
- More **efficiently** reduce IOP than β-blockers - Systemic side effects are not significant
35
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?
- 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
Which α2-agonist is the first line agent for the treatment of glaucoma?
Brimonidine
37
Why is the α2-agonist, Apraclonidine, not preferred for the treatment of glaucoma?
Frequent allergic reactions, development of tachyphylaxis
38
What is the MOA of α2-agonists in tx of glaucoma?
**Decrease** the **rate** of **aqueous humor production**
39
What are the adverse systemic and local effects of α2-agonists used in the treatment of glaucoma?
- **Systemic:** dizziness, fatigue, dry mouth, bradycardia, reduced BP - **Local:** allergic reaction (eyelid edema, itching, hyperemia)
40
What is the algorithm for pharmacotherapy of open angle glaucoma?
- 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
With closed angle glaucoma the goal is a rapid reduction of IOP, what drugs are used in preparation for surgery?
- Systemic osmotic diuretics: **IV Mannitol (1-2 g/kg)** - **Pilocarpine** = drug of choise before surgery - induces **miosis**
42
What occurs during surgery for a closed angle glaucoma?
Produce a hole in the iris facilitating the humor outflow (iridectomy)
43
What 3 drugs are contraindicated with open angle glaucoma?
1. Glucocorticoids (topical, systemic, nasal, inhaled) 2. Fenoldopam 3. Topic antimuscarinic drugs
44
Which drugs are contraindicated with closed angle glaucoma due to their ability to cause mydriasis and possible angle closure?
- **Antimuscarinic drugs** (topical, systemic) - Drugs w/ **alpha-adrenomimetic activity** (topical) - **Tricyclic antidepressants** and **Serotonin-norepinephrine reuptake inhibitors** (due to potent antimuscarinic action)

Ahmed Neuro 2 Depression (16 decks)

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