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28 Cards in this Set
- Front
- Back
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What is CFU?
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Colony forming unit
A measure of viable bacteria numbers |
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What is MIC?
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Minimum inhibitory concentration
the lowest conc of a drug that produces no apparent bacterial growth |
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Common Pathogens for ADULTS?
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1. Staphylococcus (gram +)
2. Streptococcus (gram +) 3 Pseudomonas (gram -) 4 Enterobacteria (gram -) |
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Common Pathogens for KIDS?
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1.H. Flu (82%)
2.Strep pneumonia 3.Staph Aureus |
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In the Ocular TRUST study, what was the only antibiotic that was effective against MRSA?
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Trimethoprim
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What is the advantage of a liposome or microsphere in drug delivery?
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Liposomes:
1. bioerodible and biocompatible systems consisting of microscopic vesicles composed of lipid bilayers surrounding aqueous compartments. 2. demonstrated prolonged drug effect at the site of action but with reduced toxicity. |
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Why are sulfa drugs inactivated by mucopurulent d/C?
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Sulfa and PABA are very similar structurally. Pus contains PABA. therefore, if there is pus present (mucopurulent d/c), there is a lot of PABA around, and the PABA competes with sulfa so the sulfa can't get to the appropriate receptors and inhibit the bacteria's growth.
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What is the advantage of having BAK in an antibiotic?
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BAK alone, bactericidal activity starts with in 5 mins
-reduces the tear break up time by 1/2 zymar has BAK |
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why does moxeza, zymaxid, besivance, and azasite have less dosing requirements?
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they have durasite or xanthum gum which increases contact time of drug
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Why would one antibiotic have a higher concentration in the AC than another antibiotic, if they were equal in concentration at the ocular surface?
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the drugs have different solubility properties
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Cell wall inhibitors abx?
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Penicillans
Cephalosporin bacitracin vancomycin |
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bacterial cell membrane disruption abx?
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Polymixin B
Gramicidin |
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Protein synthesis inhibitors abx?
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Tetracycline 30s
Macrolide 50s aminoglycosides 30s Chlororamphenicol |
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Folic acid synthesis inhibitors abx?
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Pyrimethamine
Sulfonamide Trimethoprim |
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DNA synthesis inhibitors abx
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Fluoroquinolones
Inhibits topoisomerase II and IV |
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Mechanism for oral anti-herpetic drugs?
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inhibits DNA synthesis
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Why do some viruses survive on inanimate surfaces while others don’t?
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Those viruses do NOT have lipid envelopes (ex – Adenovirus)
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Dosing for Acyclovir?
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HSV: 400mg, 5x a day for 7-10 days
HZV: 800mg, 5x a day for 7-10 days |
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Dosing for Valtrex?
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HSV: 1 g PO BID
HZV: 1 g PO TID |
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Acyclovir
Mechanism and structure |
• Purine analogue to guanine that is specific to viral cells
• Inhibit DNA synthesis • Short half life bc of poor GI absorption • Common side effects mostly GI |
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Valacyclovir
Mechanism and function |
• Prodrug of acyclovir
• Hydrolized by esterases in GI tract, converting valacyclovir to acyclovir, therefore making more bioavailable |
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Famvir
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-prodrug of penicyclovir
-Inhibits DNA synthesis • Well-absorbed orally • Active against HSV 1 & 2 and HZV |
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What would be reason(s) for initiating prophylactic treatment in an ocular herpes simplex patient?
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Prophylaxis against secondary bacterial infection of conj and cornea
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how do Polyenes work?
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-Bind to ergosterol
increase cell membrane permeability -fungistatic in low doses |
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How do Pyrimidines work?
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• aka antimetabolites
• Block thymidine synthesis in some fungi • Impairs DNA synthesis • Fungistatic – Flucytosine |
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How do Azoles work?
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• Impair ergosterol in cell membrane, increasing cell membrane permeability
• Fungistatic • Resistance is increasing • More interactions with other systemic drugs in this category |
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How do Echinocandins work?
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• Inhibit glucan synthesis, weaken cell wall of some fungi
• Newer class of drugs including capsofungin, micafungin, anidulafungin |
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Which azole drug has been reasonably good against yeast and can be used topically?
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1. Fluconazole: mainly effective against yeasts
2. Miconazole: relatively good activity against yeast |
