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OPHTHALMOLOGY > OCULAR DRUGS (Anti-viral,Anti-fungal,Beta blockers in Glaucoma & Prostaglandin Analogs) > Flashcards

OCULAR DRUGS (Anti-viral,Anti-fungal,Beta blockers in Glaucoma & Prostaglandin Analogs) Flashcards

1
Q

What is the route of administration for Trifluridine?

A

Ophthalmic (1% solution)

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2
Q

What is the mechanism of action of Trifluridine?

A

Fluoro-pyrimidine nucleoside analog

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3
Q

What is Trifluridine the drug of choice for?

A

Keratoconjunctivitis due to HSV-1 or HSV-2

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4
Q

What limits Trifluridine’s use?

A

Limited because of topical administration

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5
Q

What is the oral bioavailability of Acyclovir?

A

20-23%

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6
Q

What is the primary route of excretion for Acyclovir?

A

Majority excreted unchanged in urine (75%)

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7
Q

What are the mechanisms of resistance for Acyclovir?

A

Alteration in viral thymidine kinase and DNA polymerase

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8
Q

What are the clinical uses of oral Acyclovir?

A

First episode genital herpes, recurrent genital herpes, genital herpes suppression in the HIV-infected host, herpes zoster, varicella (age > 2 years)

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9
Q

What are the adverse effects of IV Acyclovir?

A

Renal insufficiency, CNS toxicity (delirium, confusion), hypersensitivity

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10
Q

What differentiates Valacyclovir from Acyclovir in pharmacokinetics?

A

Higher bioavailability (~70%) and peak serum acyclovir levels 5-6 times higher with PO valacyclovir

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11
Q

What is the bioavailability of Famciclovir?

A

~75%

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12
Q

How is Famciclovir converted to its active form?

A

Rapidly converted to penciclovir by deacetylation of the side chain and oxidation of the prior ring

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13
Q

What are the adverse effects of Famciclovir?

A

Headache, diarrhea, nausea, rash, neuropathies, hallucinations, or confusional states

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14
Q

What is the mechanism of action of Foscarnet?

A

Directly inhibits viral DNA and RNA polymerases by interacting with the pyrophosphate binding site

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15
Q

What are the clinical uses of Foscarnet?

A

CMV retinitis, colitis, esophagitis in immunocompromised patients, acyclovir-resistant HSV infections

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16
Q

What are the major toxicities associated with Foscarnet?

A

Renal insufficiency, hypokalemia, hypophosphatemia, CNS toxicity, electrolyte imbalance

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17
Q

What is the mechanism of action of Ganciclovir?

A

Inhibits DNA polymerase of CMV and HSV via phosphorylation by viral thymidine kinase

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18
Q

What are the clinical uses of Ganciclovir?

A

CMV colitis or esophagitis in HIV patients, CMV retinitis

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19
Q

What is a major side effect of systemic Ganciclovir treatment?

A

Myelosuppression

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20
Q

What is the prodrug of Ganciclovir?

A

Valganciclovir

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21
Q

What are the clinical uses of Valganciclovir?

A

Treatment of CMV infections in immunocompromised patients, CMV retinitis, CMV prophylaxis in transplant patients

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22
Q

What is the mechanism of action of Cidofovir?

A

Inhibits viral DNA synthesis by slowing and terminating chain elongation; competitive inhibitor with respect to dCTP

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23
Q

What is the primary clinical use of Cidofovir?

A

Treatment of CMV infections in immunocompromised patients

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24
Q

What is a significant adverse effect of Cidofovir?

A

Nephrotoxicity

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25
Q

What are the administration routes for Amphotericin B?

A

Ophthalmic (0.3-0.5% solution), IV (0.5-1 mg/kg), topical, subcutaneous, intrathecal, intralesional injection

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26
Q

How is Amphotericin B excreted?

A

Renal excretion (4%) and biliary excretion

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27
Q

What is the mechanism of action of Amphotericin B?

A

Binds to ergosterol in fungal cell membranes, forming cytotoxic ‘leaky pores,’ causing loss of intracellular contents

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28
Q

What is the resistance mechanism of Amphotericin B?

A

Decreased permeability or modification of ergosterol concentration at the sterol binding site

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29
Q

What is the spectrum of activity of Amphotericin B?

A

Candida spp, Cryptococcus neoformans, Aspergillus spp, Histoplasma capsulatum, Blastomyces dermatitidis, Coccidioides immitis, systemic infections, fungal meningitis

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30
Q

What are the major side effects of Amphotericin B?

A

Nephrotoxicity, infusion reactions, anemia, and electrolyte imbalances (hypokalemia, hypomagnesemia)

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31
Q

What is the route of administration for Natamycin?

A

5% topical suspension

32
Q

What is the mechanism of action of Natamycin?

A

Inhibits fungal growth by binding to ergosterol, preventing membrane formation and function

33
Q

What are the clinical uses of Natamycin?

A

Yeast and fungal keratitis, conjunctivitis

34
Q

What is the bioavailability of Fluconazole?

A

High bioavailability

35
Q

How is Fluconazole excreted?

A

Unchanged in urine

36
Q

What is the mechanism of action of Fluconazole?

A

Inhibits fungal P450-dependent enzymes, blocking ergosterol synthesis

37
Q

What are the primary clinical uses of Fluconazole?

A

Oropharyngeal candidiasis, esophageal candidiasis, vaginal candidiasis, cryptococcal meningitis

38
Q

What is the resistance mechanism of Fluconazole?

A

Can occur with long-term use, especially with prophylactic use

39
Q

What are the adverse effects of Fluconazole?

A

Nausea, headache, abdominal pain, and elevated liver enzymes

40
Q

How does Itraconazole absorption improve?

A

Improved with food due to decreased gastric pH

41
Q

Does Itraconazole cross the BBB?

A

No, CSF: serum concentration ratio is <0.01

42
Q

What is the mechanism of action of Itraconazole?

A

Inhibits fungal P450-dependent enzymes, blocking ergosterol synthesis

43
Q

What are the clinical uses of Itraconazole?

A

Dermatophytoses, endemic mycoses (Histoplasma, Blastomyces, Sporothrix), aspergillosis, and yeast keratitis

44
Q

What are the side effects of Itraconazole?

A

GI upset, hepatotoxicity, and risk of drug interactions (CYP3A4 inhibitor)

45
Q

How is Ketoconazole excreted?

A

Parent drug and metabolites excreted in feces and urine

46
Q

Does Ketoconazole cross the BBB?

A

No, CSF: serum concentration ratio is <0.1

47
Q

What is the mechanism of action of Ketoconazole?

A

Inhibits fungal P450-dependent enzymes, blocking ergosterol synthesis

48
Q

What are the clinical uses of Ketoconazole?

A

Non-meningeal cryptococcosis, mucocutaneous candidiasis, seborrheic dermatitis, and pityriasis versicolor

49
Q

What are the adverse effects of Ketoconazole?

A

Hepatotoxicity, nausea, and inhibition of steroid synthesis

50
Q

What are the routes of administration for Miconazole?

A

Topical (2% solution or ointment), intravaginal suppository (20 mg/g), IV injection

51
Q

What is the mechanism of action of Miconazole?

A

Inhibits fungal ergosterol synthesis

52
Q

What are the clinical uses of Miconazole?

A

Vulvovaginal candidiasis, dermatophytic infections (tinea cruris, tinea pedis), yeast keratitis

53
Q

What are the side effects of Miconazole?

A

Rare but may include local irritation or hypersensitivity

54
Q

What is the clinical use of Timolol?

A

Treatment of glaucoma and ocular hypertension

55
Q

What are the side effects of Timolol?

A

Localized irritation and burning, CNS effects (lethargy, lightheadedness, fatigue, memory loss), CV effects (bradycardia, hypotension, syncope, arrhythmias, bronchoconstriction, pulmonary edema, CHF, and death)

56
Q

What makes Levobunolol different from Timolol?

A

It is less expensive than Timolol

57
Q

What are the side effects of Levobunolol?

A

Localized irritation and burning, CNS effects (lethargy, lightheadedness, fatigue, memory loss), CV effects (bradycardia, hypotension, syncope, arrhythmias, bronchoconstriction, pulmonary edema, CHF, and death)

58
Q

What is a key benefit of Betaxolol compared to other beta blockers?

A

Useful in patients with CHF, asthma, or conditions where β1 blockade is contraindicated due to cardioselectivity

59
Q

What are the clinical uses of Carteolol and Metipranolol?

A

Treatment of ocular hypertension and glaucoma

60
Q

What are the side effects of Carteolol and Metipranolol?

A

Localized irritation and burning, CNS effects (lethargy, lightheadedness, fatigue, memory loss), CV effects (bradycardia, hypotension, syncope, arrhythmias, bronchoconstriction, pulmonary edema, CHF, and death)

61
Q

What is the mechanism of action of Latanoprost?

A

Increases uveoscleral aqueous outflow as an ester prodrug of PGF2α

62
Q

What are the clinical uses of Latanoprost?

A

Treatment of open-angle glaucoma

63
Q

What are the side effects of Latanoprost?

A

Burning, stinging, conjunctival hyperemia, foreign body sensation, blurred vision, and increased pigmentation of the iris (especially in green-brown, yellow-brown, and blue-gray-brown eyes after prolonged use)

64
Q

What is the half-life of Latanoprost?

A

17 minutes

65
Q

What is the mechanism of action of Bimatoprost?

A

Increases uveoscleral aqueous outflow as a prostaglandin analog

66
Q

What are the clinical uses of Bimatoprost?

A

Treatment of open-angle glaucoma

67
Q

What are the side effects of Bimatoprost?

A

Burning, stinging, conjunctival hyperemia, foreign body sensation, and blurred vision

68
Q

What is the onset of action for Travoprost?

A

2 hours

69
Q

What is the mechanism of action of Travoprost?

A

Increases uveoscleral aqueous outflow as a prostaglandin analog

70
Q

What are the side effects of Travoprost?

A

Burning, stinging, conjunctival hyperemia, foreign body sensation, and blurred vision

71
Q

What is the onset of action for Unoprostone?

A

30 minutes

72
Q

What is the mechanism of action of Unoprostone?

A

Increases uveoscleral aqueous outflow as a docosanoid compound related to a PGF2α metabolite

73
Q

What are the side effects of Unoprostone?

A

Burning, stinging, conjunctival hyperemia, foreign body sensation, and blurred vision

74
Q

What is the duration of action for Latanoprost, Bimatoprost, and Travoprost?

A

24 hours

75
Q

What is the clinical use of Unoprostone?

A

Treatment of open-angle glaucoma

OPHTHALMOLOGY (4 decks)

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