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35 Cards in this Set
- Front
- Back
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What is selective toxicity? |
Weak spots in a pathogen that are selective to that organism. |
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Name 6 drugs/classes of drugs that target bacterial cell wall. Hint: VAMPCC |
Vacomycin Ampicillin Methicillin Penicillin Cephalosporins Clavulanic Acid |
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Where do most antibacterial drugs come from (in nature)? |
From fungi (because they have evolved to protect themselves from bacteria) |
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What does ciprofloxacin target? Describe the mechanism of action. |
Bacterial topoisomerase By inhibiting topoisomerase, it promotes the breakage of double-stranded DNA. |
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T/F: Ciprofloxacin may also attack the human topoisomerase, causing unwanted side effects. |
False, it is specific for the bacterial topoisomerase. |
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What pharmacologic category does ciprofloxacin correspond to? |
Antibiotic, fluoroquinolone. |
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What does rifampin target? Describe the mechanism of action. |
Bacterial RNA polymerase It inhibits transcription (mRNA) |
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Describe the mechanism of action of sulfonamides and trimethoprim. |
They block tetrahydrofolate synthesis pathway (which is required to make thymidine, a major building block of DNA), thus inhibiting DNA synthesis. |
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Why don't sulfonamides and trimethoprim affect human DNA synthesis as well? |
Because we get folate from diet, we don't synthesize it (we don't have the pathway that is inhibited by those drugs) |
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T/F: The ribosomes of eukaryotes and prokaryotes are the same. |
False. They are different, this is why we have many drugs that target and inhibit bacterial protein synthesis. |
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What do chloramphenicol and erythromycin target? |
The 50s subunit of bacterial ribosomes, thus inhibiting protein synthesis. |
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What do tetracycline and aminoglycosides target? |
The 30s subunit of bacterial ribosomes, thus inhibiting protein synthesis. |
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What is empirical therapy? |
You don't know what the bacteria is, so you prescribe a "broad spectrum antibiotic". |
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What is definite therapy? |
Targets specific bacteria. |
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When is prophylactic therapy typically used? |
Post-surgery. (Broad-spectrum AbX) |
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What is the MIC (minimal inhibitory concentration)? |
The concentration of drug that stops bacteria from growing (min. concentrations that "clears" a test tube) |
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What is the MBC (minimal bactericidal concentration)? |
The concentration of drug that KILLS the bacteria (min. concetration that "clears" the agar plate) |
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How may one determine the MIC and the MBC? |
By doing the dilution test (tubes and agar) |
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What is the difference between a bactericidal agent and a bacteriostatic agent? |
Bactericidal: kills Bacteriostatic: stops growth |
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T/F: Bacteriostatic agents are good for use in immunocompromised pts. |
False! It can cause bacterial proliferation. Use bactericidals instead. |
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Why should one not use both bactericidal and bacteriostatic agents at the same time? |
Because bactericidal agents act only during cell division. If division does not happen (e.g. in the case of bacteriostatic agent use), they are ineffective. Thus, in immunocompromised pts, there is a risk of overgrowth of bacteria and... infection. |
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Name 3 mechanisms of drug resistance in bacteria. |
1. Mutation 2. Plasmid-based 3. Interspecies recombination |
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How likely is it for a mutation to occur in bacteria? (#) |
1 in 1 million bacteria |
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How is mutational resistance acquired? |
After cell division, one strain becomes resistant (1/2 daughters = resistant), while the other 1/2 = sensitive. The resistant population keeps on growing while the sensitive one succumbs to the drug. |
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How is plasmid resistance acquired? |
A resistant bacteria meets a sensitive one and, through fusion, transfer and separation, they share plasmid DNA and acquire resistance. |
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T/F: Mutational resistance is acquired much faster than plasmid resistance. |
False. Plasmid resistance is acquired much faster than mutational resistance. |
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How is resistance through recombination acquired? |
Two bacteria share chromosomes; |
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What enzyme does penicillin target? |
Transpeptidase. (or Penicillin-binding protein) |
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T/F: If ppl stay in one place, chance of bacterial resistance decreases. |
True. |
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T/F: Smaller populations increase the chance of conferring resistance. |
False. Larger population do* |
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How does climate change impact the reemergence of infectious diseases? |
Increase in temperature is advantageous for bacterial proliferation. |
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T/F: Monotherapy increases the number of resistant strains in bacteria. |
True. Risk increases by 1 in a million with each mono-therapeutic drug given to the pt. |
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What is the main concern one has regarding the use of combination Abx therapy? |
The creation of super-resistance. Although it is more likely for this to occur in monotherapy. |
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Why is the combination of Aminoglycosides and cell wall inhibitors synergistic? |
Aminoglycosides cannot kill bacteria because it cannot cross the cell wall. Giving a cell wall inhibitor Abx can enable the action of Aminoglycosides. |
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How do Aminoglycosides act? |
They cause a.a. mismatching and, thus, stop protein synthesis. |
