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Neurology Week 4 > Ocular Pharmacology > Flashcards

Ocular Pharmacology Flashcards

1
Q
A
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2
Q

What are the main ocular muscarinic antagonists?

A

Atropine

Cyclopentolate

Homotropine

Scopolamine

Tropicamide

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3
Q

What are the main ocular muscarinic agonists?

A

Carbachol

Pilocarpine

Acetylcholine HCl

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4
Q

What are the main ocular AchE inhibitors?

A

Echothiphate

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5
Q

What are the main ocular sympathomimetics?

A

Dipivefin

Phenylephrine

Apraclonidine

Brimonidine

Naphazoline

Tetrahydrozoline

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6
Q

What are the main ocular PG analogs?

A

Latanoprost

Travoprost

Bimatoprost

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7
Q

What are the main ocular Beta-adrenergic antagonists?

A

Timolol maleate

Levobunolol

Metipranolol

Carteolol

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8
Q

What are the main ocular CA Inhibitors?

A

Acetazolamide

Dorzolamide

Brinzolamide

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9
Q

What are the main drugs for macular degeneration?

A

Aflibercept

Pegaptanib

Ranibizumab

Bevacizumab

Verteporfin

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10
Q

Anatomy of the eye

A

Enlargement of the anterior segment, revealing the cornea, angle structures, lens, and ciliary body

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11
Q

What are the roles of the ciliary body?

A
  • secretion of aqueous humor by the epithelial bilayter
  • accommodation by the ciliary muscle
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12
Q

What is the effect of a1 binding in the iris radial muscle?

A

mydriasis (sympathetic)

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13
Q

What is the effect of M3 binding in the iris sphincter muscle?

A

miosis (parsym)

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14
Q

What receptors are found in the corneal epithelium? endothelial?

A

Epithelial- B2 and Ma- effects unknown

Endothelium- B2- effects unknown

Ma= although acetylcholine and choline acetyltransferase are abundnat in the corneal epithelium of most species, the function of this NTM is unknown here

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15
Q

What receptors are found in the trabecular meshwork?

A

B2- effects unknown

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16
Q

What receptors are found in the ciliary epithelium?

A

a2/B2- binding causes aqueous production

The ciliary epithelium is also the target of CA inhibitors (CA isoenzyme II is localized to both the pigmented and nonpigmented ciliary epithelium)

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17
Q

What receptors are found in the ciliary muscle?

A

B2= relaxation

M3= accommodation

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18
Q

What receptors are found in the lacrimal gland?

A

a1= secretion (adrenergic)

M2,M3= secretion (cholinergic)

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19
Q

What receptors are found in the retinal pigment epithelium?

A

a1/B2= H2O transport/unknown

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20
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21
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22
Q

What plants are known to contain natural antimuscarinics (will cause mydriasis if topically applied to the eye)?

A

Datura or Angel’s Trumpets (below)

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23
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A
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24
Q

What ocular rxn can canthaxanthine cause?

A

crystalline retinopathy

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25
Q

What ocular rxn can chamomile cause?

A

conjunctivitis (probable when topically applied)

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26
Q

What would be the effect of working with this plant and then rubbing ones eye?

A

Datura- mydriasis (unilateral)

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27
Q

What would be the effect of touching this plant and then touching your eyes?

A

Echinaeca- conjunctivitis (possible, not certain)

28
Q

What are some possible ocular effects of ginkgo biloba?

A

retinal hemorrhage

hyphema

retrolobular hemorrhage

29
Q

What candy can cause abnormal vision?

A

licorice

30
Q

How can niacin affect the eye?

A

cystoid macular edema (certain)

blurred vision (probable)

31
Q

How can vitA affect the eye?

A

intracranial HTN (certain in large doses)

32
Q

How do opiods cause miosis?

A

The pupilloconstrictor (Edinger-Westphal nucleus) neurons are spontaneously active pacemaker cells. Nociceptor input activates inhibitory neurons which counteract this miosis.

Opiates (as well as slow wave sleep and in general anesthesia) block the action of the inhibitory neuron, resulting in miosis

33
Q

What are some possible routes of distribution following topical admin of a drug in the eyes?

A

If the admin is too large in volume or too frequent, some can spill onto the cheeks where vasaoconstriction and obvious skin discoloration can occur

Well applied, small, lipophilic drugs will be absorbed via the cornea

Large, hydrophilic molecules will be primarily absorbed via a non-corneal route in the eye or via systemic absorption via the lacrimal drainage system into the nasal mucosa, and into the GI tract (main route)

34
Q

Describe topical admin of eye drugs

A

prompt absorption, depending on formulation

convenient, economical, safe

compliance, corneal, nasal and conjunctival toxicity, and systemic AEs limit use

35
Q

Describe subconjunctival, sub-Tenon’s, and retrobulbar injection admin of eye drugs

A

prompt or sustained absorption, depending on formulation

good for anterior segment infections, posterior uveitis, and cystoid macular edema

Local toxicity, tissue injury, globe perforation, optic nerve trauma, central retinal a./v. occlusion, and prolonged drug effect limit use

36
Q

Describe intraocular admin of eye drugs

A

prompt absorption

good for anterior segment surgery, infections

corneal toxicity, intraocular toxicity, and relatively short DOA limit use

37
Q

Describe intravitreal injection or device admin of eye drugs

A

absorption circumvented, immediate local effect, potential sustained effect

good fo endophthalmitis, retinitis, age-related macular degeneration

retinal toxicity limits use

38
Q

What ocular drugs are pro-drugs?

A

Dipivefrin HCl,a prodrug for epi

Latanoprost, a prodrug for PGF2

both are used for glaucoma tx

39
Q

Muscarinic antagonists (e.g. atropine, homotropine, tropicamide, cycopentolate, scopolamine) are used to produce cycloplegia (loss of accommodation) and adaptation (mydriasis). Describe these and their clinical sues

A
  • may produce transient and localized irriation following application (increased IOP)
  • used to tx iris/uveal tract inflammatoru conditions and for eye exams

drug systemization can cause dry mouth, photophobia, tachycardia, palpitations, HA, and somnolence

40
Q

Muscarinic antagonists are contraindicated in who?

A

glaucome pts and with sulfite preservative allergies (interrupt the flow of aqueous humor)

41
Q

Aqueous humor is normally produced and drained at the same rates, keeping a constant IOP. If drainage is impaired, glaucoma can result (compression of the retina and optic nerve damage)

NOTE: Aqueous humor maintains the shape and pressure within the globe. What is Tonometry?

A

the method of measuring IOP using calibrated instruments (normal: 10-21 mmHg)

42
Q

How is open angle glaucoma tx?

A

decrease AH production or increase outflow

43
Q

How is closed angle glaucoma tx?

A

surgical iridectomy; short-term medical management to decrease IOP and clear the cornea prior to surgery

44
Q
A
45
Q

Decisions in how to tx glaucoma

A

Can use either mitotic drugs or anticholinesterases, but each have their own AEs

46
Q

What are the major drug classes used to tx glaucoma?

A

1st line: Prostaglandin analogs (latanoprost, travoprost, etc.)

B-receptor antagonists (timolol maleate, levobunolol, carteolol)

CA II Inhibitors (acetazolamide, dorzolamide, brinzolamide)

47
Q

How do PGF2a analogs work to tx glaucoma?

A

They are products that undergo hydrolysis but the MOA is unclear (thought to promote aqueous outlfow via accessory iveoscleral pathways)

48
Q

What are the AEs of PGF2a analogs?

A

Acute: blurred vision, burning, itching

Chronically: slow and permanet brown pigmentation of the iris, eyelid skin, and eyelashed; also increasing their growth in length and thickness (used in a product called latisse (bimatoprost), to thicken eyelashes)

49
Q

How do BBs tx glaucoma?

A

inhibit the production of aqueous humor via either decreasing cAMP-PKA stimulation or reducing ocular bloodflow and ultrafiltration

Rapid effect and sustained action

50
Q

75-90% of ciliary body epithelium and blood vessel receptors are ___

A

B2

51
Q

How do CAII inhibitors help tx glaucoma?

A

by reducing bicarbonate secretion and fluid transport to decrease IOP

52
Q

What are the AEs of CAII inhibitors?

A

localized rxns; ocular irritation, burning, stinging

bacterial keratitis from bacterial contamination in multi-dose containers

25% experience dysgeusia-bitter taste via inhibition of CA in the oral cavity

blurred vision, lacrimation, photophobia, and xreophthalmia

allergic rxns (sulfonamides)- agranulocytosis, aplastic anemia, SJS, TEN, gulminant hepatic necrosis

53
Q

What are the uses of muscarinic agonists and cholinesterase inhibitors?

A

increase aqueous humor flow (formerly DOC for glaucoma; since replaced by BB);

contraindicated with constriction undesirable (e.g. iritis, uveitis, inflammatory conditions of the anterior chamber)

54
Q

What are the AEs of muscarinic agonists and cholinesterase inhibitors?

A

transient stinging, tearign, decreased night vision (caution in ots with cholinergic-mediated medical conditions (CV failure, asthma, peptic ulcer GI spasm)

55
Q

T or F. Cholinesterase inhibitors (Echthiophate) are more potent and longer-acting than direct acting miotics

A

T. But AEs are more common (additive effects with carbamate and organophosphate toxicity-insecticides). Contraindicated in closed-ange glaumoca (increase IOP)

56
Q

What is the use of dipivefrin?

A

E receptor pro-drug for tx of glacuoma

57
Q

What is the use of phenylephrine?

A

a binding for induction of mydriasis, vasoconstriction, and decongestion

58
Q

What is the use of apraclonidine?

A

a2 binding for ocular HTN tx

59
Q

What is the use of brimonidine?

A

a2 binding for tx of glaucoma, ocular HTN

60
Q

What is the use of Naphazoline and tetrahydrozoline?

A

a binding for action as a decongestant

61
Q

How do sympathomimetics act in the eye?

A

They all reduce IOP by improving the outflow of aqueous humor

62
Q

What are the AEs of sympathomimetics?

A

photosenstivity, conjunctival hyperemia, and hypersensitivity

used with caution in HTN, hyperthyroidism, diabetes, asthma, and artheriosclerosis

63
Q

How is macular degeneration tx?

A

Intravitreal injection of a decoy VEGF receptor (Aflibercept), a VEGF antagonist (Pegaptanib), or MAB (Ranibizumab, Bevacizumab) to interrupt vascular spread over the retina

64
Q

What are the AEs of macular degeneration tx drugs?

A

arterial thromboembolism

nonfatal stroke

nonfatal MI

vascular necrosis

65
Q

What is Veteporfin used to tx?

A

macular degeneration, via producing free radicals when activated by a laser, resulting in damage of blood vessels and preventing neovascularization

66
Q

What are the AEs of Veteporfin?

A

HE, injection site rxns

temporary photosensitization (avoid exposure of the skin or eyes to direct sunlight for 5 days)

Neurology Week 4 (26 decks)

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