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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

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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
What are the administration routes for Amphotericin B?
Ophthalmic (0.3-0.5% solution), IV (0.5-1 mg/kg), topical, subcutaneous, intrathecal, intralesional injection
26
How is Amphotericin B excreted?
Renal excretion (4%) and biliary excretion
27
What is the mechanism of action of Amphotericin B?
Binds to ergosterol in fungal cell membranes, forming cytotoxic 'leaky pores,' causing loss of intracellular contents
28
What is the resistance mechanism of Amphotericin B?
Decreased permeability or modification of ergosterol concentration at the sterol binding site
29
What is the spectrum of activity of Amphotericin B?
Candida spp, Cryptococcus neoformans, Aspergillus spp, Histoplasma capsulatum, Blastomyces dermatitidis, Coccidioides immitis, systemic infections, fungal meningitis
30
What are the major side effects of Amphotericin B?
Nephrotoxicity, infusion reactions, anemia, and electrolyte imbalances (hypokalemia, hypomagnesemia)
31
What is the route of administration for Natamycin?
5% topical suspension
32
What is the mechanism of action of Natamycin?
Inhibits fungal growth by binding to ergosterol, preventing membrane formation and function
33
What are the clinical uses of Natamycin?
Yeast and fungal keratitis, conjunctivitis
34
What is the bioavailability of Fluconazole?
High bioavailability
35
How is Fluconazole excreted?
Unchanged in urine
36
What is the mechanism of action of Fluconazole?
Inhibits fungal P450-dependent enzymes, blocking ergosterol synthesis
37
What are the primary clinical uses of Fluconazole?
Oropharyngeal candidiasis, esophageal candidiasis, vaginal candidiasis, cryptococcal meningitis
38
What is the resistance mechanism of Fluconazole?
Can occur with long-term use, especially with prophylactic use
39
What are the adverse effects of Fluconazole?
Nausea, headache, abdominal pain, and elevated liver enzymes
40
How does Itraconazole absorption improve?
Improved with food due to decreased gastric pH
41
Does Itraconazole cross the BBB?
No, CSF: serum concentration ratio is <0.01
42
What is the mechanism of action of Itraconazole?
Inhibits fungal P450-dependent enzymes, blocking ergosterol synthesis
43
What are the clinical uses of Itraconazole?
Dermatophytoses, endemic mycoses (Histoplasma, Blastomyces, Sporothrix), aspergillosis, and yeast keratitis
44
What are the side effects of Itraconazole?
GI upset, hepatotoxicity, and risk of drug interactions (CYP3A4 inhibitor)
45
How is Ketoconazole excreted?
Parent drug and metabolites excreted in feces and urine
46
Does Ketoconazole cross the BBB?
No, CSF: serum concentration ratio is <0.1
47
What is the mechanism of action of Ketoconazole?
Inhibits fungal P450-dependent enzymes, blocking ergosterol synthesis
48
What are the clinical uses of Ketoconazole?
Non-meningeal cryptococcosis, mucocutaneous candidiasis, seborrheic dermatitis, and pityriasis versicolor
49
What are the adverse effects of Ketoconazole?
Hepatotoxicity, nausea, and inhibition of steroid synthesis
50
What are the routes of administration for Miconazole?
Topical (2% solution or ointment), intravaginal suppository (20 mg/g), IV injection
51
What is the mechanism of action of Miconazole?
Inhibits fungal ergosterol synthesis
52
What are the clinical uses of Miconazole?
Vulvovaginal candidiasis, dermatophytic infections (tinea cruris, tinea pedis), yeast keratitis
53
What are the side effects of Miconazole?
Rare but may include local irritation or hypersensitivity
54
What is the clinical use of Timolol?
Treatment of glaucoma and ocular hypertension
55
What are the side effects of Timolol?
Localized irritation and burning, CNS effects (lethargy, lightheadedness, fatigue, memory loss), CV effects (bradycardia, hypotension, syncope, arrhythmias, bronchoconstriction, pulmonary edema, CHF, and death)
56
What makes Levobunolol different from Timolol?
It is less expensive than Timolol
57
What are the side effects of Levobunolol?
Localized irritation and burning, CNS effects (lethargy, lightheadedness, fatigue, memory loss), CV effects (bradycardia, hypotension, syncope, arrhythmias, bronchoconstriction, pulmonary edema, CHF, and death)
58
What is a key benefit of Betaxolol compared to other beta blockers?
Useful in patients with CHF, asthma, or conditions where β1 blockade is contraindicated due to cardioselectivity
59
What are the clinical uses of Carteolol and Metipranolol?
Treatment of ocular hypertension and glaucoma
60
What are the side effects of Carteolol and Metipranolol?
Localized irritation and burning, CNS effects (lethargy, lightheadedness, fatigue, memory loss), CV effects (bradycardia, hypotension, syncope, arrhythmias, bronchoconstriction, pulmonary edema, CHF, and death)
61
What is the mechanism of action of Latanoprost?
Increases uveoscleral aqueous outflow as an ester prodrug of PGF2α
62
What are the clinical uses of Latanoprost?
Treatment of open-angle glaucoma
63
What are the side effects of Latanoprost?
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
What is the half-life of Latanoprost?
17 minutes
65
What is the mechanism of action of Bimatoprost?
Increases uveoscleral aqueous outflow as a prostaglandin analog
66
What are the clinical uses of Bimatoprost?
Treatment of open-angle glaucoma
67
What are the side effects of Bimatoprost?
Burning, stinging, conjunctival hyperemia, foreign body sensation, and blurred vision
68
What is the onset of action for Travoprost?
2 hours
69
What is the mechanism of action of Travoprost?
Increases uveoscleral aqueous outflow as a prostaglandin analog
70
What are the side effects of Travoprost?
Burning, stinging, conjunctival hyperemia, foreign body sensation, and blurred vision
71
What is the onset of action for Unoprostone?
30 minutes
72
What is the mechanism of action of Unoprostone?
Increases uveoscleral aqueous outflow as a docosanoid compound related to a PGF2α metabolite
73
What are the side effects of Unoprostone?
Burning, stinging, conjunctival hyperemia, foreign body sensation, and blurred vision
74
What is the duration of action for Latanoprost, Bimatoprost, and Travoprost?
24 hours
75
What is the clinical use of Unoprostone?
Treatment of open-angle glaucoma

OPHTHALMOLOGY (4 decks)

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