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Ocular Pharmacology > Glaucoma Agents > Flashcards

Glaucoma Agents Flashcards

1
Q

If bicarbonate is in pH below it’s pKa will it be mostly ionized or non-ionized?

A

Non-ionized (In component form)

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2
Q

If bicarbonate is in pH above it’s pKa will it be mostly ionized or non-ionized?

A

Ionized (Acid form)

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3
Q

True or false, the acidosis caused by CAIs is part of the mechanism of action to lowering IOP

A

False

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4
Q

What are the systemically administered CAIs?

A

Acetalzolamide (Diamox)

Methazolamide (Neptazane)

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5
Q

What are the topically administered CAIs?

A

Dorzolamide (Trusopt) 2%
Brinzolamide (Azopt) 1%
Cosopt; 2% dorzolamide and 0.5% timolol

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6
Q

Describe the ocular effects with CAIs

A

DECREASE IN IOP VIA DECREASING AQUEOUS PRODUCTION

Metabolic acidosis

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7
Q

What effect will CAIs have on a normal non-glaucoma patient’s eye?

A

None

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8
Q

What’s the normal dose and onset for Diamox?

A

125-250mg 4X a day; 3-4 hours for max effect lasting 6-12 hours

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9
Q

What’s the normal dose for Diamox Sequels?

A

500mg 1-2x a day; lasts 18-24 hours

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10
Q

How long does Diamox need to take effect if given by IV?

A

30 minutes, lasts 2-4 hours

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11
Q

What’s the max effectiveness for oral methazolamide?

A

Taken 2x a day, after 7-8 hours for max effect and duration is 10-14 hours

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12
Q

Describe the toxicities seen with CAIs

A 
Very common, dropout is 20-30%
Parathesia; tingling/pins and needle sensation in the extremities that also can cause abnormal taste
Headache, fatigue, dizziness, drowsy
GI; Irritation, upset, cramping, weight loss,  NVD, anorexia
Muscle weakness and decreased libido
Lethargy, depression and malaise
Diuresis via K+ depletion
Renal and colic stones
Transient myopia
Rarely aplastic anemia
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13
Q

What are the contraindications for CAIs?

A 
SULFA DRUG ALLERGY
Renal dysfunction
Hypokalemia
Liver cirrhosis
Severe COPD (can develop respiratory alkalosis and be unable to maintain increased respiratory rate)
Renal calculi (kidney stone)
Pregnancy
Do not use for chronic non-congestive angle closure
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14
Q

With topical dorzolamide, do you see the drift effect seen with beta blockers like Timolol?

A

No

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15
Q

How does the brinzolamide (azopt) suspension compare to the use of the topical drop dorzolamide?

A

Brinzolamide 1% suspension taken 2-3x day equals 2% dorzolamide 3x day
Less dose and systemic toxicity

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16
Q

What two drugs are in cosopt and how does cosopt’s efficacy compare to the agents comprising it alone?

A

2% dorzolamide and 0.5% timolol

More effective than either agent alone

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17
Q

Describe ocular toxicities with dorzolamide

A

Short term keratitis/mild irritation

Burning, blurry vision, FBS, ocular allergies less likely with brinzolamide

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18
Q

What is a possible corneal toxicity with dorzolamide or other similar topical CAIs?

A

Corneal edema or even corneal decomposition

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19
Q

If your patient has a history of an intraocular surgery such as a corneal transplant, what concern would arise from selecting a topical CAI?

A

Corneal endothelium compromise

20
Q

Describe some systemic toxicities with dorzolamide

A

Sulfa allergy
Bitter taste
Headache
Concern with patients with compromised/history of compromised liver and/or kidney

21
Q

Between a topical CAI (Dorzolamide) and a beta blocker (Timolol) which has better diurnal control of IOP?

A

Topical CAI

22
Q

Name the class of drug that is now the gold standard for newly diagnosed glaucoma patients

A

Prostaglandin Analogs

23
Q

Describe the MOA for Latanoprost

A

PGF2a analog; prodrug until esterases at cornea convert to active drug to then work at proper receptor
Increases UVEOSCLERAL OUTFLOW, as well as causing substantial remodeling of TM to reduce resistance to outflow via increasing MMP production to break down the TM’s extracellular matrix

24
Q

What kind of tolerance/drift/absorption effects are present with Latanoprost (other prostaglandins)

A

No tolerance develops
IOP well controlled (equal to or better than Timolol 2x day)
No drift
No effect from iris color, age, race, sex, previous treatments, or type of glaucoma to be treated

25
Q

Describe some toxicities with Latanoprost (Xalatan) and other prostaglandins

A 
HYPEREMIA OF CONJUNCTIVA
Blurred vision, stinging eyes (related to increased inflammation due to stimulating prostaglandin receptors)
FBS, punctate keratopathy
Cystoid macular edema
Corneal pseudodendrites (herpes simplex)
Seemingly no systemic toxicities
26
Q

Describe the permanent and non-permanent cosmetic toxicity seen with Latanoprost and other prostaglandins

A

Permanent - Increase in Iris melanin formation (darker eye)

Non-permanent - thicker and longer eyelashes

27
Q

What are the contraindications for Latanoprost and other prostaglandins?

A

Hypersensitivity to drug or drug components (Sulfa)

28
Q

What are some cautions for prescribing for Latanoprost and other prostaglandins?

A

Ocular inflammation

Or a history of aphakia, pseudoaphakia with torn posterior capsule or cystoid macular edema

29
Q

What is the name for the “synthetic prostamide analog”?

A

Bimatoprost (Lumigan) 0.03%, 0.01%

30
Q

For the treatment of glaucoma with Bimatoprost (lumigan) would it help to go from 0.01% to 0.03%?

A

Not really, both concentrations seem to be equally effective but the 0.01% tends to have less toxicities (by a bit)

31
Q

What is the name for the formulation of Bimatoprost (lumigan) used for cosmetics?

A

Latisse 0.03% for hypotrichosis (eyelash ‘deficiency’)

32
Q

Compare Latanoprost (Xalatan) with Travoprost (Travatan) in terms of MOA.

A

MOA for Latanaprost (Xalatan) and Travaprost (Travatan) are the same; PGF2alpha analog

33
Q

Describe Travatan Z

A

Travaprost (Travatan) uses a different preservative and is ‘preservative free’ by being less irritating to the cornea.

34
Q

Compare Latanoprost (Xalatan) with Tafluprost (Zioptan) in terms of MOA and preparation

A

Both are still prostaglandin analogs; PGF2alpha.

Tafluprost is used as a single drop dispensing with no preservatices

35
Q

Describe Neuroprotectin as a method to treat glaucoma

A

Newer method tested in animal models, Nitrogen Oxide Synthesis Inhibitors; decreases cell apoptosis –> protecting neurons from dying in glaucoma

36
Q

Describe the A2 agonist Brimonidine (alphagan) in the treatment of glaucoma

A

Seemed to help in cases of retinal ischemia in preventing cell death in animal studies

37
Q

What is Aminoguanidine being used to treat in animal studies?

A

Glaucoma

38
Q

Describe Memantine (used to treat Alzheimer’s) in the treatment of glaucoma

A

NMDA receptor blocker; prevent excessive glutamate on NMDA receptor to prevent excitotoxicity (apoptosis from excessive stimulation)
Shown to decrease nerve cell loss in retina and LGN in monkeys

39
Q

Describe Resveratrol in the treatment of glaucoma; and mention where it can be found.

A

Antioxidant found in abundance in red wine

Decreases cell death IN VIVO; perhaps neuroprotective in nature

40
Q

Describe the general MOA and name the prototypical Hyperosmotic Agent used for treating glaucoma

A

Agents that cause greatly increased plasma osmolarity and effectively dehydrate body tissues like the eye (mainly vitreous) and CSF

Mannitol

41
Q

Describe the use of hyperosmotic agents

A

Used for acute angle closure glaucoma and pre/post surgery

42
Q

Describe the toxicities seen with the use of all Hyperosmotic Agents

A

Decreased CSF volume causing headache
Dry mouth and increased thirst
Nausea and Vomiting
Hyperosmotic coma from excessive CNS dehydration
Congestive Heart Failure and/or Pulmonary Edema from increased cardiac load
Muscle cramping and weakness if given IV

43
Q

Which is the drug of choice for IV hyperosmotics?

A

Mannitol; takes 30-60 minutes for peak efficacy lasting 6-8 hours

44
Q

Describe the Glycerin (Osmoglyn)

A

Oral hyperosmotic, max effect in 5 hours

Caution for diabetic patients as this has a caloric value (super sweet sugar water)

45
Q

Briefly, describe the IOP lowering effects of Ethanol and Marijuana

A

EtOH - Osmotic effect like osmotic diuretics
Marijuana - Possible cannabinoid receptor action to lower IOP, or may just be the lowering of BP in general causing lower IOP. Not terribly effective due to requiring constant use for IOP reduction. (Might be fun though)

Ocular Pharmacology (11 decks)

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