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34 Cards in this Set

  • Front
  • Back
What are chemotherapeutic agents?
Chemotherapeutic agents are chemical agents that are used to treat disease.
Why do they need to be selectively toxic?
They need to be selectively toxic so that they harm the invading organism to a greater extent than the host.
What is the therapeutic index?
The therapeutic index is the ratio of the toxic dose to the therapeutic dose. (the larger the index the better (toxic = low))
Define antibiotic.
An antibiotic is a microbial product or derivative that can kill susceptible microorganisms or inhibit their growth.
What are synthetic and semi-synthetic antimicrobial agents?
Synthetic antimicrobial agents are man-made substances that inhibit the growth of or kill microbes. Semi-synthetic antimicrobial agents are modified antibiotics.
How do broad spectrum antibiotics differ from narrow spectrum antibiotics?
Broad spectrum antibiotics effect a wide variety of organism, usually both gram-negative and gram-positive, while narrow spectrum antibiotics effect a limited variety of organisms.
What type of answer does the Kirby-Bauer susceptibility test give and what do S, I, and R mean?
The Kirby-Bauer susceptibility test gives a qualitative answer. S stands for susceptible, I stands for intermediate, and R stands for resistant.
How are MIC and MBC values determined?
The MIC and MBC values are determined by a series of dilutions; computerized systems make this process much easier.
What do MIC and MBC stand for?
The MIC is the Minimum Inhibitory Concentration and the MBC is the Minimum Bacteriocidal Concentration.
What is the advantage of these assyays over the Kirby-Bauer?
The advantage of dilution assays over the Kirby-Bauer is that you get a quantitative answer, instead of just qualitative.
How may the choice of an agent depend not only on in vitro susceptibility results but also on the route of administration, the site of infection, and the rate of clearance?
The choice of an agent partly depends on: the route of administration, becasue the drug must be able to reach the site of infection, the site of infection, because things such as blood clots, nectotic tissue, and the blood brain barrier may not allow agents to reach the site, and the rate of clearance, because the rate of clearance can determine the concentration of the agent which can determine effectiveness.
What are the general mechanisms of drug resistance (at least 6)?
The general mechanisms of drug resistance are: 1) state of growth (transient), 2) change target, 3) modify antibiotic, 4)deny access to target, 5) metabolic compensation, and 6) failure to activate (MNE).
Which mechanisms are temporary (transient)?
The 'state of growth' mechanism is temporary (transient).
Which mechanisms usually arise by a mutation?
The mechanism of 'denying access to the target' usually arises by a mutation in the drug receptor so that the antibiotic can't bind and inhibit.
Which mechanisms are commonly the result of a gene transfer?
The mechanism of 'modifying the antibiotic/agent' is commonly the result of a gene transfer.
What are R factors?
R factors are plasmids bearing one or more resistance gene.
What problem has arisen from the administration of antibiotics to farmstock?
Widespread antibiotics has arisen form the administration of antibiotics to farmstock.
What are the mode of action of the B-lactams, vancomycin, and bacitracin?
It has been proposed that B-lactams inhbit the enzyme catalyzing the transpeptidation reaction because of their structural similarity, which would bloch the synthesis of a complete, fully cross-linked pg and lead to osmotic lysis. Vancomycin blocks pg synthesis by inhibiting the transpeptidation step that cross-links adjacent pg strands (addition of disaccharide-pentapeptide to backbone chain); leads to weak pg and osmotic lysis. Bacitracin effects/prevents the recycling of bactoprenol in pg synthesis by preventing phosphorylation.
What are the two families of the B-lactams?
Two families of B-lactams are penicillins and cephalosporins.
How is resistance to the B-lactams generally acquired?
Resistance to B-lactams is generally acquired by gene transfer of a gene that encodes for the enzyme B-lactamase, which modifies/inactivates the B-lactams.
What are four inhibitors of protein synthesis and their targets?
Four inhibitors of protein synthesis are 1) aminoglycosides which bind to the 30S subunit of the ribosome, 2) tetracyclines which also bind to the 30S subunit of the ribosome, 3) chloramphenicol, which binds the 23S rRNA of the 50S subunit of the ribosome, and 4) macrolides, wich binds the 50S subunit of the ribosome.
Why are the aminoglycosides bacteriocidal while tetracycline is bacteriostatic
Why might erythromycin be prefered over chloramphenicol?
Erythromycin might be prefered over chloramphenicol because it is non-toxic while the latter is highly toxic (causes blood disorders).
What structure/processes are the targets of the polyenes and the imidazoles?
Polyenes insert into sterol membranes and form pores. Imidazoles inhibit sterol synthesis and disrupt membrane permeability.
Why are these specific to fungi?
Do the polyenes have a high or a low therapeutic index?
Polyenes have a low therapeutic index because they can insert into cholesterol membranes.
What is the pathway affected by the sulfonamide and trimethoprim (in lecture) antimetabolites and why are they often give together?
Sulfonamides and trimethoprims interupt the production of folic acide which bacteria must synthesize for purine and pyrimidine syntheisis and they are often given together because each interupt the cycle at a different point, so if any intermediate makes it by the sulfonamide the trimethoprim will take care of it.
Why are these selectively toxic?
What is the mode of action of amantadine, which is useful in the protection against Influenza A?
Amantadine binds influenza A M2 ion channel which prevents the acidification of the virion which stops fusion of the phagosome with the lysosme.
What is the target of Relenza and Tamiflu?
Relenza and Tamiflu inhibit neuraminidase, which allows the virus to be released when budding off occurs
What are the inhibitors of nucleic acid synthesis and their targets (e.g. gyrase, RNA polymerase, etc.)?
The inhibtors of nucleic acid synthesis are: Quinolones inhibit gyrase (double stranded breaks), Rifampin inhibits RNA polymerase (stops transcription), Griseofulvin disrupts mitotic spindles, 5-flucytosine is converted to 5-fluorouracil and incorporated into RNA (can't be translated).
What is the molecular target of griseofulvin?
The molecular target of griseofulvin are the mitotic spindles.
What confers the specificity of action to the nucleoside (base) analogs 5-flucytosine, AZT, and acyclovir?
5-flucytosine is converted by the fungi to 5-fluorouracil which is incorporated into the RNA and stops translastion. AZT interferes with reverse transcriptase activity and blocks the reproduction of retroviruses. Acyclovir is converted from its inactive to active form by the virus itself. Each of these is transformed by the target and then elicits its response.
What are the targets of NRTIs, NNRTIs, PIs, and Fusion Inhibitors?
NRTIs (Nucleoside Reverse Transcriptase Inhibitors) targets the enzyme reverse transcriptase (3'-OH deficient chain terminators=errors). NNRTIs (Non-Nucleoside RT Inhibitors) inhibit RT allosterically. PIs (Protease Inhibitors) target the enzyme protease (mimics peptide bond-competitive inhibition). Fusion Inhibitors block GP41-mediated fusion w/host cell receptor.