! Neuro Eye Pharm Flashcards

(52 cards)

1
Q

B blocking drugs

A
Betaxolol
Timolol
Metripranolol
Levobunonol
Carteolol
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2
Q

A2 adrenergic agonists

A

Apraclondine

Brimonidine

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3
Q

Prostagladin analogs

A

Latanoprost
Bimatoprost
Travoprost

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4
Q

Carbonic anhydrase inhibitors

A

Topical-brinzolamide, dorzolamide

Systemic-acetazolamide, methazolamide

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5
Q

Muscarinicagonists

A

Carbachol

Pilocarpine

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6
Q

Inhibitors of cholinesterase

A

Demecarium

Echothiophate

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7
Q

Iris circular muscle

A

Constricts pupil to cause miosis

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8
Q

Iris radial muscle

A

Dilated pupil to cause mydriasis

Effect is due to activation of a1 adrenergic receptors

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9
Q

Ciliary muscle

A

Causes accommodation of the eye to near vision
Opens up trabecular meshwork, improves outflow of aqueous humor into the canal of s helm, decreasing intraocular pressure

M3 receptors contract the muscle

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10
Q

Ciliary epithelium

A

Produces (secretes) aqueous humor

B receptor activation increases humor production

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11
Q

Ciliary body

A

Secretes aqueous humor

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12
Q

How does aqueous humor flow

A

Into space in front of iris through trabecular meshwork and exits via canal of schlemm

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13
Q

Blocking b adrenoreceptors associated with ciliary epithelium

A

Decreases secretion. Of aqueous humor

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14
Q

Blood vessels

A

In sclera arealso under autonomic control and influence aqueous drainag

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15
Q

B receptors and aqueous humor

A

Increase

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16
Q

A2 receptors and aqueous humor

A

Decrease

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17
Q

Carbonic anhydrase

A

Aqueous humor?

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18
Q

Contraction of ciliary muscle and aqueous humor 9muscarinic)

A

Improved outflow

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19
Q

Contraction of iris circulat muscle, (muscarinic)

A

Miosis an improved outflow

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20
Q

____ improves uveoscleral, or unconventional outflow

A

Prostagladin F2a

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21
Q

Contraction of iris radial muscle (a1), mydriasis

A

Decreased outflow (conventional outflow)

22
Q

Glaucoma

A

Group of ocular disorders that lead to an optic neuropathy associated with loss of visual sensitivity and field

23
Q

Whites or African Americans get glaucoma more

24
Q

Open or closed angle glaucoma more common

25
When should a patient be treated for glaucoma
Increased IOP and optic disc changes and/or visual field defects
26
Goal of glaucoma treatment
Reduce IOP by 30% want is less than 21 mmHg
27
If two glaucoma meds are given. How far apart should administration be
Ten minutes
28
Does initial response to therapy dictate long term
No
29
If agents are to be changed
One day overlap
30
First line agents open angle glaucoma
Prostagladin analogues B blockers-timolol Brimonidine
31
Second line therapy open angle glaucoma
Pilocarpine Apraclonidine Topical carbonic anhydrase inhibitors
32
Last line therapy open angle glaucoma
Carbachol Inhibitors of cholinesterase Oral carbonic anhydrase
33
Why are B blockers used
Convince of dosing few side effects
34
Why is timolol the preferred beta blockers
Lacks local anesthetic effects (propranolol local anesthetic properties0 Generically available Full antagonist As effective as pilocarpine
35
MOAtimolol
Reducing the production of aqueous humor by the ciliary body by blocking B receptors
36
Adverse local effects of beta blockers
``` Stinging Dry eyes Blurred vision Blepharitis, keratiti, conjunctivitis -could be due to other things in the formulation and not the B blockers ```
37
Systemic adverse effects of b blockers
Can get systemic absorption Heart-negative inotropy effect, bradycardia Airway-bronchospasm Hyperlipidemia Exacerbation of hypoglycemia May interact with orally given verapamil-increase risk of cardiac depression and heart block Use with caution in patients with bradycardia, AV block heart failure, atherosclerosis, diabetes,
38
Prostagladin analogues
Latanoprost Bimatoprost Travoprost
39
Which prostagladin is most effective at lower IOP
Bimatoprost
40
Prostagladin analogues for IOP
More effective than B blockers Given once daily at nighttime (1 drop) Systemic side effects are not significant
41
Local side effects prostagladin analog
Corneal erosions Conjunctival hypermedia Iris hyperpigmentation(several months of therapy and is irreversible) Hypertrichosis, hyperpigmentation around eye lashes and eyelids are reversible upon discontinuation of therapy
42
A2 agonists
Brimonidine-first line agent | Apraclonidine-frequent allergic reactions, development of tachyphylaxis
43
MOA a2 agonists
Decrease the rate of aqueous humor production
44
Adverse effects a2 agonists
Systemic-dizzy, Antigua, dry mouth, bradycardia, reduced blood pressure
45
Locals adverse effect a2 agonists
Allergic reaction (eyelid edema, itching, hypermedia)
46
How treat open angle glaucoma
1. B blocker 2. If intolerant to b blocker, use class alternative 3. If contraindications to b blockers, switch to brimonidine or prostagladin 4. If intolerance to prostagladin, use class alternative 5. If contraindications to all first class agents,use topical carbonic anhydrase inhibitors (2nd line) - if monotherapy fails, use a combo - if intolerance or inadequate response to the combination therapy, use laser or a surgical procedure
47
Goal of treating closed angle glaucoma
Rapid reduction of IOP
48
Acute treat closed angle
Use systemic osmotic diuretics in preparation for surgery (IV mannitol)
49
Pilocarpine
Drug of choice for closed angle before surgery. It inducedmiosis
50
Surgical or laser iridectomy for closed angle
Produce a hole in the iris facilitating the humor outflow
51
What drugs are contraindicated in open angle
Glucocorticoids Fenoldopam Topical anti muscarinic drugs
52
Drugs contraindicated in closed angle (angle closure may be triggered by any drug that causes mydriasis)
Antimuscarinic drugs (topical, systemic) Drugs with alpha adrenomimetics activity (topical) Tricyclic antidepressants and serotonin-NE reuptake inhibitors (because of their potent antimuscarinic action)