Drugs for Glaucoma (Konorev) Flashcards

1
Q

What do the Iris Circular M. and Iris Radial M. do in the eye?

What receptor activation leads to each of their effects?

How do these muscles affect the flow of aqueous humor?

A

Circular: constricts pupil = MIOSIS

  • Receptor = M3 (Gq protein coupled)
  • improved outflow of humor

Radial: dilates pupil = MYDRIASIS

  • Receptor = a1 (Gq protein coupled)
  • reduced outflow of humor
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2
Q

What is the function of the Ciliary M. and what receptor causes its contraction?

A

ACCOMMODATION of the eye for NEAR VISION
- Receptor = M3 (contracts the muscle; Gq coupled)

  • opens trabecular meshwork, improves aqueous humor loss = DECREASED intraocular pressure
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3
Q

What is the function of Ciliary Epithelium and what two receptors does it have?

A

Produces AQUEOUS HUMOR

  • B receptors (Gs coupled) = INCREASE humor prod.
  • a2 receptor (Gi coupled) = DECREASE humor prod.
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4
Q

How does Carbonic Anhydrase play a role in Intraocular Pressure?

A

CA transports sodium/bicarbonate ions from ciliary body to aqueous humor

  • inc. osmotic pressure of humor enhances water transport to humor = INC VOLUME
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5
Q

What molecule improves uveoscleral outflow of aqueous humor and how does presynaptic a2 receptor activation do the same?

A

Prostaglandin F2alpha improves uveoscleral outflow

  • presynaptic a2 receptors relax the ciliary muscle = inc. uveoscleral outflow
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6
Q

What is the difference between Primary Open Angle Glaucoma and Primary Closed Angle Glaucoma?

A

OAG = chronic progressive disease w/NO apparent mechanical blockage of humor outflow
- 95% of all cases

CAG = acute intermittent partial/complete blockage of outflow
- 5% of all cases

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7
Q

What are the 4 classes of drugs used to REDUCE AQUEOUS HUMOR PRODUCTION in Open Angle Glaucoma?

(B/A/CT/CS)

A
  1. Beta-blocking Drugs (“-olol”)
  2. a2 adrenergic agonists (“-onidine”)
  3. Topical Carbonic Anhydrase Inhibitors
    • Brinzolamide and Dorzolamide
  4. Systemic Carbonic Anhydrase Inhibitors
    • Acetazolamide and Methazolamide
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8
Q

What are the 4 classes of drugs used to INCREASE AQUEOUS HUMOR OUTFLOW in Open Angle Glaucoma?

(P/A/D/CI)

A
  1. Prostaglandin analogs (“-oprost”)
  2. a2 adrenergic agonists (“-onidine”)
  3. Direct cholinergic agonists
    • Carbachol and Pilocarpine
  4. Cholinesterase Inhibitors (Indirect cholinergic agon.)
    • Echothiophate
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9
Q

Which Beta Blocker is most commonly used to treat Glaucoma and why?

A

TIMOLOL
- lacks local anesthetic effects and is a full antagonist

antagonizes B receptors of ciliary body = dec. aqueous humor production

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10
Q

How do Beta Blockers interact with Calcium Channel Blockers?

A
  • inc. risk of cardiac depression and heart block
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11
Q

What are the two a2 agonists used to treat Glaucoma (B/A) and what are their two MOAs?

A

Brimonidine and Apraclonidine (“-onidine”)
- Apraclonidine INFREQUENTLY USED = allergies

  1. dec. aqueous humor production
  2. dec. ACh release by activating PRE-SYNAPTIC a2 ciliary muscle receptors = relaxation
    • this INCREASES UVEOSCLERAL OUTFLOW
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12
Q

What are the two Topical Carbonic Anhydrase Inhibitors (B/D) and two Systemic Carbonic Anhydrase Inhibitors (A/M)?

A

Topical = Brinzolamide, Dorzolamide
- more commonly used for long-term therapy

Systemic = Acetazolamide, Methazolamide
- often intolerable upon long-term use

  • “-zolamide”
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13
Q

What Prostaglandin Analog is MOST effective in lowering IOP and what is the common suffix of this class of drugs?

What is the MOA and side effects of use of these drugs?

A

BIMATOPROST is most effective at lowering IOP
- can be given 1x/day and is better than Beta Blockers

  • inc. uveoscleral outflow and less extent conventional outflow

SE: local side effects that change eye appearance w/use = hypertrichosis/hyperpigmentation
- reversible after therapy discontinuation

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14
Q

What are the two Direct Cholinergic Agonists (P/C) and what is the Indirection Cholinergic Agonist (E) used to treat Glaucoma?

What are two side effects of long-term use?

A
Direct = Pilocarpine and Carbachol
Indirect = Echothiophate
  • both cause inc. conventional outflow (either by stimulating M3 receptors or inc. ACh at receptor sites)

SE: cataracts and iris-lens adhesions

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15
Q

What is the plan of treatment for Open Angle Glaucoma and what is the Nasolacrimal Duct Occlusion Technique?

A
  1. start w/Beta Blocker or Prostaglandin agent
    • if intolerance to specific agent, use a class alternate
  2. switch to brimonidine or topical CAI if BB/P are BOTH contraindicated
  3. if monotherapy fails –> use combo therapy
  4. if combotherapy fails –> use laser/surgery

NDOT = pressure for 3 min over nasolacrimal sac after drops are applied

  • dec. drainage of meds = no systemic spread
  • inc. local concentration of meds
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16
Q

What is the difference between Closed Angle Glaucoma WITH pupillary block vs Closed Angle Glaucoma WITHOUT pupillary block?

A

PB: tight iris-lens contact blocks humor flow to Ant. Chamber –> iris moves forward and blocks outflow

WPB: ciliary processes push iris forward, blocking outflow; especially during MYDRIASIS

17
Q

What two systemic osmotic diuretics are used to prep for surgery in patients with Closed Angle Glaucoma?

What drug is given BEFORE surgery to induce miosis?

What 3 drug classes help reduce humor production in Closed Angle Glaucoma?

A

Prep = Oral Glycerin and IV Mannitol
- both help take water out of the eye

Miosis = PILOCARPINE

Reduce humor: B blockers, a2 agonists, Carbonic Anhydrase Inhibitors

18
Q

Drug Induced Glaucoma

What are two drugs that promote IOP elevation in:

  1. Pts. with OPEN Angle Glaucoma
  2. Pts. with CLOSED Angle Glaucoma
A
  1. Glucocorticoids and Topical Antimuscarinic drugs
  2. a1 adrenomimetic and antimuscarinic drugs
    • anti-M drugs = SNRI and TCA

CAG –> any drugs that cause MYDRIASIS