Glaucoma Meds Flashcards

1
Q

What causes the pupil to constrict?

A

iris circular muscle

M3 receptor

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2
Q

What causes the pupil to dilate?

A

iris radial muscle

alpha 1

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3
Q

What causes accommodation of the eye to near vision and decreases intraocular pressure (improves outflow of aqueous humor)?

A

ciliary muscle

M3

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4
Q

What produces aqueous humor?

A

ciliary epithelium

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5
Q

What activation increases humor production?

A

beta adrenergic

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6
Q

What receptor activation decreases humor production?

A

alpha 2

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7
Q

What does carbonic anhydrase do to aqueous humor?

A

transports sodium and bicarb from ciliary body into humor

increases osmotic pressure, enhances water transport to humor–>increases volume

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8
Q

What improves outflow of aqueous humor?

A

contraction of ciliary muscle

contraction of iris circular muscle (constriction of pupil)

both M3

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9
Q

What improves unconventional aqueous humor outflow?

A

prostaglandin F2a

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10
Q

What does sympathetic nervous system do to eye?

A

dilates pupil via contraction of iris radial muscle (decrease outflow)
–> alpha 1

relax ciliary muscle (increase uveoscleral outflow)
–> alpha 2

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11
Q

Define glaucoma

A

ocular disorders–> optic neuropathy a/w loss of visual sensitivity and field

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12
Q

What types of glaucoma are there?

A

primary (genetic, congenital)

  • -> open angle glaucoma most common: progressive disease without mechanical blockage to humor outflow
  • -> closed angle glaucoma: acute intermittent partial or complete blockage of outflow (emergency to avoid vision loss)

secondary (disease, trauma, surgery, drug-induced)

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13
Q

What is the most common form of glaucoma?

A

open-angle (no known outflow blockage)

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14
Q

What is one factor that can cause open angle glaucoma?

A

increased IOP–> optic neuropathy (damage to optic nerve)

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15
Q

Generally, what drugs reduce the amount of aqueous humor produced?

A

beta blockers (olol)

alpha 2 agonists (idine)

carbonic anhydrase inhibitors (amide)

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16
Q

Generally, what drugs increase aqueous humor outflow?

A

prostaglandin analog (oprost)

alpha 2 agonist (idine)

direct cholinergic agonist

inhibitors of cholinesterase

17
Q

Why is Timolol favored in glaucoma?

A

lacks local anesthetic effects

generic

full antagonist

18
Q

Why are beta blockers used?

A

convenience of dosing

general lack of local adverse effects

19
Q

Beta blocker MOA

A

reduce production of humor by ciliary body

20
Q

Local adverse effects of beta blockers

A

little, usually well tolerated

ocular irritation
dry eyes

21
Q

Systemic adverse effects of beta blockers

A

bradycardia

bronchospasm

hyperlipidemia

hypoglycemia

interact with calcium blockers

careful with use in cardiac patients

22
Q

What is the main alpha 2 agonist used in glaucoma?

A

brimonidine

23
Q

Alpha 2 agonist MOA

A

decrease humor production

increase uveoscleral outflow (unconventional) via relaxing ciliary muscle

24
Q

Side effects of alpha 2 agonists

A

systemic: headache, fatigue, dry mouth
local: eyelid edema, itching, hyperemia (allergic rxn)

25
Q

MOA of carbonic anhydrase inhibitors

A

-lamide

decrease osmotic pressure of humor

26
Q

Side effects of carbonic anhydrase inhibitors

A

local–> ocular irritation and redness

systemic: N, diarrhea, altered taste, weight loss, paresthesia, renal stones, decreased libido

intolerable with long-term use

27
Q

MOA of prostaglandin analogs

A

-oprost

reduce IOP via increased uveoscleral and conventional outflow of humor

28
Q

Why give prostaglandin analogs for glaucoma?

A

once at nighttime

more efficiently reduce IOP c/t beta blockers

29
Q

Adverse effects of prostaglandin analogs

A

systemic not significant

local: corneal erosions, hyperemia, iris hyperpigmentation (irreversible with months of use), hypertrichosis of eye lashes that is reversible with d/c

30
Q

What are direct-acting cholinergic agonists?

A

pilocarpine

carbachol

31
Q

What are indirect-acting cholinergic agonists (AKA inhibit cholinesterase)?

A

echothiophate

32
Q

MOA of cholinergic agonists

A

activate M3 directly or indirectly (inhibit cholinesterase)–> elevate Ach levels

increases conventional humor outflow

33
Q

Adverse effects of cholinergic agonists

A

systemic rare

local: ha, periorbital pain, constriction of pupil with diminished night vision, eyelid twitching, myopia, cataracts with long-term use, iris-lens adhesions with long-term use

34
Q

How to treat glaucoma

A

beta blocker or prostaglandin first

if intolerant: use class alternative

if contraindications to both: brimonidine or topical carbonic anhydrase inhibitor

combo therapy

laser or surgical procedure

35
Q

Describe pupillary block closed angle glaucoma

A

tight contact between iris and lens–> flow of humor into anterior chamber blocked–> iris moves forward and blocks outflow

36
Q

Describe closed angle glaucoma without pupillary block

A

ciliary processes located in such a way that they push the iris forward–> blocks outflow, especially when pupil is dilated

37
Q

Goals for treatment of closed angle glaucoma

A

medical emergency to keep vision

  • -> reduce IOP with oral glycerin or IV mannitol to prep for surgery
  • -> pilocarpine before surgery induces constriction of pupil
  • -> reduce humor production via beta blocker, alpha 2 agonist or carbonic anhydrase inhibitor
38
Q

What drugs promote elevation of IOP?

A

open angle glaucoma patients: glucocorticoids, topical antimuscarinic drugs

closed angle glaucoma patients, cause dilation of pupil: alpha 1, antimuscarinic drugs