Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Ocular Pharmacology > Exam 3 Pharm Material: Ocular Hypotensive Drugs/Ocular Hyperosmotic Drugs > Flashcards

Exam 3 Pharm Material: Ocular Hypotensive Drugs/Ocular Hyperosmotic Drugs Flashcards

1
Q

What is the general path of aqueous production and outflow?

A

Aqueous is produced by the ciliary epithelium and is secreted into the posterior chamber. The aqueous flows through the pupil into the anterior chamber and follows the convection current towards the trabecular meshwork. The trabecular meshwork accounts for 80-90% of outflow through the conventional pathway that travels through the TM into Schlemm’s canal and then to the episcleral venous plexus. The other 10-20% of aqueous outflow occurs through uveoscleral outflow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the autonomic system impact aqueous production and outflow?

A

Production: Sympathetic innervation of the CB alpha receptors decreases production. Innervation of beta receptors on the CB increases production.

Outflow: Parasympathetic innervation of M3 receptors on the iris sphincter and causes contraction. This contraction will cause miosis and stretch the TM, increasing outflow. Parasympathetic innervation of M2 receptors of the longitudinal muscle of the CB causes contraction. This contraction will pull on the scleral spur, increasing outflow.

Production: Sympathetic ONLY
Outflow: Parasympathetic ONLY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the different hypotensive drug classes? What are their cap colors?

A 
Cholinergic Agonists/Miotics: Dark Green
Beta-Blockers: Yellow: 0.5% Light Blue: 0.25% 
Alpha Adrenergic Agonists: Purple 
Prostaglandin Analogs: Turquoise 
Carbonic Anhydrase Inhibitors: Orange 
Rho-Kinase Inhibitors: White?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the MOA of cholinergic agonists?

A

Bind to the M3 receptors of the iris sphincter muscle causing miosis. Miosis will stretch the TM increasing outflow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the direct-acting cholinergic agonists? What does direct-acting mean?

A

Isopto carpine/Pilocarpine
Pilopine HS/Pilocarpine HCL (gel)
Direct-acting means they act on the receptors themselves and stimulate the receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are cholinergic agonists particularly useful for?

A

Narrow/closed-angle glaucoma. Miosis pulls the peripheral iris away from the angle increasing outflow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some side effects of cholinergic agonists?

A

Headache, blurred vision, narrowing angle, retinal detachment

Blurred vision can occur due to less light being let in due to miotic pupil.
Angle narrowing can occur because as the ciliary body muscles contracts the iris is pushed forward and causes angle-closure.
Retinal detachment can occur due to increased tension on the peripheral retina due to the ciliary body contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the indirect cholinergic agonist? What is the side effect that is unique to this drug?

A

Phospholine Iodide/Echothiophate. It is clinically indicated for accommodative esotropia.
Echothiophate can cause the same side effects as pilocarpine/pilocarpine HCL but it also can cause iris cysts. These cysts can cause a pupillary block.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When does maximum IOP decrease occur with cholinergic agonists?

A

2 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the MOA of a beta-blocker?

A

Blocks beta 2 receptors and beta 1 receptors reducing aqueous production.
(Betoptic/Betaxelol is selective for beta 1 receptors, this makes betaxolol cardioselective)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the true contraindications of the nonselective beta-blockers? (3)

A

Atrioventricular Block
Sinus bradycardia
Obstructive pulmonary disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What phenomenon are beta-blockers known for?

A

Short term escape and long term drift

Short term escape: Sudden sharp increase in IOP after several weeks of treatment.
Long term drift: Receptor tolerance develops after months or years of use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When do beta-blockers have little to no effect?

A

At night, usually dosed in the morning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the different beta-blockers? (7)

A

Betagan/Levobunolol hydrochloride
Betimol/timolol hemihydrate
Betoptic-S/betaxolol hydrochloride (Beta-1 Selective)
Istalol/Timolol maleate
Optipranolol/metipranolol (not used often)
Timoptic/Timolol maleate
Timoptic XE/Timolol maleate gel-forming solution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How much do beta-blockers reduce IOP by (%)?

A

20-30% reduction

Only 15-20% with Betoptic-S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How much do cholinergic agonists reduce IOP by (%)?

A

Echothiophate & Pilocarpine: 15-25%

Pilocarpine HCL: 20-30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the common dosages for beta-blockers?

A

QD-BID, but most effective if QD in morning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the common dosages for cholinergic agonists?

A

QD-BID for echothiophate

BID-QID for pilocarpine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the MOA of Carbonic Anhydrase Inhibitors?

A

Inhibit carbonic anhydrase in the ciliary processes to decrease bicarbonate. This decreases sodium and fluid movement decreasing aqueous production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the different CAI’s?

A

Brinzolamide/Azopt
Dorzolamide/Trusopt
Aetazolamide/Diamox
Methazolamide/Naptazane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the side effects of beta-blockers? (5)

A 
Bronchospasm
Hypotension 
Bradycardia
Depression
Lethargy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are contraindications for TOPICAL CAI use?

A 
Sulfa allergy
Compromised cornea (Fuch's/Transplant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the contraindications for ORAL CAI use?

A

Liver disease
Pregnancy
Kidney disease (or stones)
Sulfa Allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What specific isoenzyme do CAI’s inhibit?

A

Isoenzyme CA-II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the dosage of a CAI if used as monotherapy? What is the dosage of a CAI if used in adjunct with a BB or PGA?

A

Monotherapy: TID
Adjunct: BID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which topical CAI will be more likely to cause blurred vision? Which topical CAI will be more likely to sting upon instillation?

A

Blurred Vision: Azopt/Brinzolamide (Suspension)

Stinging: Trusopt/Dorzolamide (5.6 pH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are oral CAI’s used for?

A

Fast IOP reduction. Examples include acute angle closure or pupillary block glaucoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the adverse effect of oral CAI’s? (Not contraindications)

A

Transient myopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the MOA of alpha 2 adrenergic agonists?

A

Bind to alpha 2 receptors on the ciliary body, decreasing Na/K+ ATPase and reducing aqueous humor production.
Brimonidine also increases uveoscleral outflow but NOT apraclonidine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the different alpha 2 adrenergic agonists?

A

Alphagan P/Brimonidine

Iopidine/Apraclonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

By how much do CAI’s reduce IOP (%)?

A

15-20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

By how much do alpha 2 adrenergic agonists reduce IOP (%)?

A

Up to 25-26% (Brimonidine 26%, Apraclonidine 25%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the side effects of alpha 2 adrenergic agonists?

A

Dry mouth
Follicular conjunctivitis (patients may report increased discomfort when putting drops in as time goes on)
Mydriasis
ALLERGY (Apraclonidine > Brimonidine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the contraindications for using alpha 2 adrenergic agonists to treat glaucoma?

A
  1. Children under 6 or weighing less than 20kg (increased systemic the side effects like lethargy, hypotension, bradycardia, etc)
  2. Patients using monoamine oxidase inhibitors for depression
  3. Patients with severe cardiac disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are some precautions when prescribing alpha 2 adrenergic agonists for glaucoma treatment?

A

Concurrent depression
Reynaud phenomenon
Orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which alpha 2 adrenergic agonist may have neuroprotective properties?

A

Alphagan P/Brimonidine, this means that brimonidine may be good for patients with stable IOP but are continuing to get worse.

37
Q

Which alpha 2 adrenergic agonists penetrates the BBB?

A

Alphagan P/Brimonidine

38
Q

Why are alpha 2 adrenergic agonists not used as a monotherapy/first-line treatment for glaucoma?

A

They have a large range of efficacy. The trough of efficacy is 14%, and the peak is 28%. This means that dosing must be very consistent (every 6-8 hours) in order to maintain adequate effect on IOP.

39
Q

What is the dosing of alpha 2 adrenergic agonists if used as adjunctive therapy with a BB or PGA?

A

BID, once upon wakening and once 8 hours later

40
Q

What is the difference between Alphagan-P and generic brimonidine?

A

Alphagan-P is preserved with purite and brimonidine is preserved with BAK. Purite is less harmful to the cornea than BAK.

41
Q

What specific side effect is very common in alpha 2 adrenergic agonists?

A

Allergic reaction can occur up to 8 months after initiating treatment.
0.2% Alphagan-P/Brimonidine = 30% of patients with reaction
Alphagan P 0.15% = 20% of patients with reaction
Alphagan P 0.1% = Allergic reaction in 10% of patients

42
Q

What are the indications for apraclonidine? Why is apraclonidine not used long term?

A

Clinical indications: Decrease risk of IOP spike peri-surgery.
Not used long term due to more redness and tachyphylaxis (decrease efficacy) when used longer than one month

43
Q

What is the MOA of Prostaglandin Analogs?

A

Increases uveoscleral outflow by binding F2 alpha receptors in the ciliary body.

44
Q

What are the different prostaglandin analogs? (6)

A 
Lumigan/Bimatoprost
Travatan Z/Travoprost
Xalatan/Iatanoprost
Zioptan/Tafluprost
Vyzalta/Iatanoprostene bunod (PGA + NOS)
Xelpros/Latanoprost emulsion
45
Q

What are the contraindications for PGA’s?

A

History of ocular inflammation (prostaglandins stimulate inflammation)
History of CME or risk of CME
History of HSV
Unilateral therapy

46
Q

What are the side effects of PGAs?

A

Periorbital fat atrophy = Sunken in appearance
Eyelash lengthening
Skin depigmentation
Makes eyes darker

47
Q

What is the typical IOP reduction of PGAs?

48
Q

Which PGA contains a warning that it may darken eye color? (3)

A

Lumiagn/Bimatoprost
Travatan Z/Travoprost
Xalatan/Iatanoprost

49
Q

Which PGA carries a warning that there is a risk for CME?

A

Zioptan/Tafluprost

50
Q

How often are PGA’s dosed?

A

Once per day, oftentimes at night

51
Q

How long does it take for PGA’s to take effect?

A

2 weeks to have full effect. This means you would not prescribe this for acute angle-closure or to reduce IOP quickly

52
Q

Which PGA would you prescribe for a patient who has a BAK intolerance?

A

Travatan Z/Travoprost, it is preserved with SofZia which is less toxic than BAK.

53
Q

Which PGA is preservative-free?

A

Zioptan/Tafluprost, expensive though

54
Q

What is the MOA of Vyzulta? What is Vyzulta?

A

Vyzulta is latanoprostene bunod, which is a combination of a PGA and a Nitric Oxide Synthase. This is a dual mechanism drug (NOT A COMBO) that increases both uveoscleral outflow and trabecular outflow.

55
Q

What does a 1mmHg reduction in IOP correlate with relating to % risk of glaucoma progression?

A

1mmHg = 10% risk of glaucoma progression. So a 1mmHg decrease lowers your risk by 10%.

56
Q

According to Melton and Thomas, what is the clinical guide to incorporating Vyzulta in glaucoma treatment?

A
  1. Try to reduce IOP with PGA by as much as possible
    2a. Add a BB to PGA if target IOP is nearly reached with PGA alone
    2b. Use Vyzulta if the patient has asthma or is a BB nonresponder
  2. When PGA + BB does not reach target IOP, consider replacing PGA with Vyzulta
57
Q

What is the drug class that specifically targets the TM?

A

Rho-Kinase Inhibitors:

Rhopressa/netarsudil

58
Q

What is the dosing of Rho-kinase inhibitors?

A

QD, in evening

59
Q

What are the side effects of Rho-kinase inhibitors?

A

Hyperemia, conjunctival hemorrhage, corneal verticillata

60
Q

What are the 3 MOAs of Rho-kinase Inhibitors?

A
  1. Increase trabecular outflow
  2. Decrease episcleral venous pressure
  3. Decrease aqueous production
61
Q

Which drug causes significant hyperemia and can cause petechial hemorrhages?

A

Rho-kinase Inhibitors

62
Q

What are the different combo drugs for the treatment of glaucoma?

A

Combigan:
Timolol + Brimonidine: Inc outflow, Dec production
BB + A2A
Cosopt:
Timolol + Drozolamide: Dec Production x2
BB + CAI
Rocklatan:
Rhopressa + Latanoprost: Inc Outflow x2, Dec Production
RK + PGA
Simbrinza:
Brimonidine + Brinzolamide: Dec Production, Inc outflow
CAI + A2A

63
Q

What is the dosage for Combigan?

64
Q

What is the dosage for Cosopt?

65
Q

What is the dosage of Rocklatan?

A

QHS (Before bed)

66
Q

What is the dosage for Simbrinza?

67
Q

Which combo drug is available in a generic?

A

Cospt is available generically in a bottle but unidose is still branded.

68
Q

Which combo drug is available as a suspension? What does this mean?

A

Simbrinza, but you must shake it before using it!

69
Q

How much does Rhopressa/Netarsudil reduce IOP by?

70
Q

What are the clinical indications for systemic ophthalmic hyperosmotic agents?

A

Treatment of highly elevated IOP (40mmHg+)

Alternative to oral CAI’s if they are contraindicated

71
Q

What are the MOAs of hyperosmotic agents?

A

Increase plasma osmotic pressure, this draws water into the blood and reduces pressure.
Reduces intraocular fluid volume (vitreous included) decreasing IOP.

72
Q

What are the systemic hyperosmotic agents used to treat elevated IOP?

A

Glycerol oral solution/Glycerin/Osmoglyn

Mannitor/Osmitrol

73
Q

What is the dosage of Glycerol oral solution?

A

1-2g/kg body weight by mouth

74
Q

What are the contraindications of glycerol oral solutions? (4)

A
  1. Hypersensitivity
  2. Diabetes (SUPER high sugar content)
  3. Elderly/Dehydrated
  4. Congestive heart disease, renal disease, confused mental states
75
Q

What are the adverse effects of glycerol oral solution? (6)

A 
Mild headache
Thirst
Nausea
Vomiting
Diarrhea 
Dizziness
76
Q

What is the clinical indication of mannitol/osmitrol?

A

Pre-operative IOP reduction

77
Q

What is the dosage of Mannitol/Osmitrol?

A

0.25-2g/kg IV 60-90 mins before surgery

78
Q

How long does it take for glycerol oral solution to take effect? How long does the effect last?

A

Takes 10-30 minutes to decrease IOP and lasts 4-8 hours

79
Q

How long does Mannitol/Osmitrol take to have an effect on IOP? How long does the effect last?

A

Takes 15 minutes to decrease IOP and lasts up to 8 hours

80
Q

What are contraindications to Mannitol/Osmitrol?

A

Anuria (non-passage of urine due to kidney failure), CHF

81
Q

What are the clinical indications for topical hyperosmotic agents?

A

Reduce corneal edema NOT reduce IOP.

82
Q

What is the MOA of topical hyperosmotic agents?

A

Draws fluid from the cornea by increasing osmolarity of the tear film.

83
Q

What are the two topical hyperosmotic agents?

A

Glycerin/Ophthalgan

Sodium Chloride/Muro128

84
Q

How long does it take for glycerin/ophthalgan to reduce corneal edema?

A

1-2 minutes

85
Q

What are the most frequent uses of glycerin/ophthalgan?

A

Acute angle-closure glaucoma
Bullous keratopathy
Fuch’s corneal dystrophy

86
Q

What is the dosage of glycerin/ophthalgan?

A

1-2 drops as needed to clear the cornea

87
Q

How long does it take sodium chloride (Muro128) to have an effect on corneal edema?

A

3-4 hours after instilling

Used for chronic corneal edema in conditions like keratoconus with hydrops or Fuch’s corneal dystrophy

88
Q

What is the dosage of sodium chloride/Muro128?

A

1gtt q3-4 hours or 0.25in ribbon in conjunctival sac q3-4 hours

Ocular Pharmacology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions