Term
| What is a substance produced by a microorganism that inhibits growth or kills other microorganisms |
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Definition
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Term
| What is the main natural role of antibiotics? |
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Definition
| Inhibition of growth of competitors (bacteria may also use for quorum sensing and signaling) |
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Term
| Introduction of ___________ is one of the major successes of modern medicine |
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Definition
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Term
________ drugs require help from the immune system to clear bacteria
________ drugs kill bacteria directly.
Can a drug be both? |
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Definition
bacteriostatic
bacteriocidal
yes- some depends on concentration/dosage (low conc=bacteriostatic; high conc=bacteriocidal) |
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Term
| Should you a patient a bactericidal drug in combination with a bacteriostatic drug? |
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Definition
| No- ex: beta-lactam drugs are cell-wall synthesis inhibitors and are bactericidal but require actively dividing bacteria (bacteriostatic drug stops cells from growing) |
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Term
What is the term for the lowest concentration of drug that will inhibit growth that is used to determine which antibiotics to use and how much to give a patient?
What is the test for this? |
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Definition
Minimal inhibitory concentration (MIC)
Etest |
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Term
How would you give in regards to the MIC if it has a concentration dependent effect and long post antibiotic effect?
How would you give a drug that is not concentration dependent and has a short post antibiotic effect? |
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Definition
Give a high concentration (above MIC) maybe once a day
give MIC concentration a few times a day |
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Term
| If you have patient and you don't know what kind of bacterial infection they have, would you use (narrow or broad) spectrum antibiotics? |
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Definition
broad (large range)
(narrow-1 or 2 types of bacteria, use when you know what you're dealing with) |
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Term
What major class of antibiotics target folic acid metabolism?
Why can they target that? |
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Definition
| Sulfa (sulfanamides) drugs (we don't make foliate, we get it from our diets) |
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Term
| What major class of antibiotics target cell wall synthesis? |
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Definition
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Term
What major class of antibiotics target DNA replication?
How do they inhibit it? |
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Definition
quinolones
Target topoisomerase (cuts DNA) and DNA gyrase (uncoiling) |
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Term
What are the 2 drugs that are given together to inhibit the conversion of PABA --> tetrahydrofolic acid?
What is this commonly used to treat and what is the biggest problem with this drug? |
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Definition
sulfonamides (competitive inhibitor) and trimethoprim (they inhibit folate synthesis)
Acne and UTIs
allergies |
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Term
| What was the first sulphadrug (only antibiotic available until after WWII) found in a synthetic red dye that acts as a prodrug? |
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Definition
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Term
Quinolones are (narrow or broad) drugs?
Are they (partially or completely) synthetic? |
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Definition
broad spectrum (not usually a first line of defense, broad spectrum leads to resistance)
completely |
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Term
What do quinolones usually end in?
How do they enter the host cell? |
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Definition
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Term
| What broad spectrum drug enters the host cells by porin and used to treat UTIs, STDs, GI, abdominal infections, and nosocomial pneumonia and but can have hepato- and cardiac toxicity |
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Definition
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Term
What position of quinolones has been modified to change activity?
What generation of quinolones would be used to treat streptococci (+)?
Which generation is effective against both TopIV and DNA gyrase? |
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Definition
R7
3rd
4th
(1st and 2nd-rarely used) |
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Term
| Do antibiotics typically work better on gram (+) or (-) bacteria? |
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Definition
| (+) because thick peptidoglycan layer (breaks cross-links) and no outer membrane |
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Term
How does penicillins (beta-lactam) work on gram (+) bacteria?
Is this reversible or irreversible? |
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Definition
| penicillin mimics the substrate for transpeptidase (enzyme that cross-links PG) and IRREVERSIBLY binds to DD transpeptidase enzyme |
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Term
What is the characteristic structure of all penicillins?
How are derivatives made? |
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Definition
4 membered beta-lactam ring
substituting the R position |
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Term
How do bacteria become resistant to penicillin?
How do we combat that? |
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Definition
they have penicillinases/beta-lactamases that cleave the beta-lactam ring=penicillin doesn't work anymore
We administer it with a b-lactamase inhibitor *clavulanate or sulbactam to prevent hydrolysis |
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Term
| What are the mechanisms of antibiotic resistance? |
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Definition
-Decrease concentration of drug in the bacteria (AB can't get into cell, efflux)
-Expression of microbial enzymes that destroy or inactivate antibiotics (beta-lactamase +)
-Alterations in microbial proteins needed to activate pro-drugs
-Mutation/ alteration of target protein
-Development of alternative pathway to that inhibited by antibiotic |
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Term
| What are the problems with penicillin drugs? |
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Definition
Rapidly excreted
Patients can be allergic
Widespread resistance in bacteria |
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Term
| Giving a beta-lactam with an aminoglycoside would be an example of? |
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Definition
| synergism (targets 2 different pathways-both bacteriocidal drugs) |
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Term
| Giving a sulfonamide with a trimethoprim would be an example of? |
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Definition
| synergism (targets 2 steps in same pathway) |
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Term
| Giving a beta-lactam and tetracycline would be an example of? |
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Definition
| antagonistic (bacteriostatic [tetracycline] blocks the bacteriocidal activity of beta-lactam) |
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Term
*List the order of resistance from least resistant to most resistant to bacterial beta-lactamases
cephalosporins
carbapenems
penicillins |
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Definition
penicillins (sensitive to b-lactamases)
cephalosporins (extended spectrum b-lactamases)
carbapenems (metallo-b-lactamases) |
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Term
| Which beta-lactam drug treats Gram (+) bacteria and has increased b-lactamases resistance and gram (-) coverage in later generations |
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Definition
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Term
| Which beta-lactam drug has the broadest spectrum antibiotic (gram + and -) and is the antibiotic of last resort for Gram - infections |
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Definition
| carbapenems (usually administered with cilastatin to inhibit breakdown of imipenen [carbapenem]) |
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Term
| What drug mimics D-alanine to inhibit the incorporation of D-alanine into peptidoglycan (instead of stopping cross linking, stops it earlier). Inhibits both G+ and G- but most commonly used to treat TB |
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Definition
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Term
| What drug is only used topically due to nephrotoxicity (for a cut) and it Inhibits the lipid carrier that brings peptidoglycan to the cell wall |
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Definition
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Term
| What drug is a last resort drug and is very difficult to develop resistance against (resistant to b-lacatamase) because it inhibits PG synthesis by binding to D-Ala-D-Ala |
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Definition
| vancomycin (used for MRSA) |
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Term
| Why is it difficult for bacteria to become resistant to vancomycin? |
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Definition
| because it inhibits PG synthesis by binding to a carbohydrate (D-Ala-D-Ala) instead of a protein that can mutate |
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Term
| What is the biggest side effect to vancomycin? |
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Definition
| dose-related hearing loss |
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Term
List the drugs that act on the ribosome.
Which is the only one that you would want to a beta-lactam drug with? why? |
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Definition
30S – aminoglycosides, tetracyclins
50S- erythromycin, clindamycin, chloramphenicol
give b-lactam with aminoglycosides because only one that is bacteriocidal (other bacteriostatic so doesn't work) |
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Term
| What organelle in the human body would be effected by a drug that acts on the ribosome? |
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Definition
| mitochondia (because ribosome is similar to bacteria) |
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Term
| What drug blocks translation elongation (A site), is bacteriostatic, broad spectrum (G+ and G-0) and the major resistance pathway is efflux? |
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Definition
tetracycline (4 rings)
-when resistant to 1 tetracyclin, resistant to all tetracycline |
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Term
| What drug is mainly used for G+, bacteriostatic, binds in the P-site of 50S ribosome and blocks the translocation of the mRNA from the A-site to the P-site? |
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Definition
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Term
Erythromycin and Azythromycin are example of what type of drug?
Which one is good for patients with penicillin allergies, broad spectrum, and taken once/day for 5 days? |
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Definition
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Term
| What drug is bacteriostatic, used against G+ and G-, binds to P site of 50S subunit of ribosome to inhibit peptidyl transferase effect (binding of single AA to growing chain) but rarely used bc serious adverse effects (anemia) except for topically in eyedrops as a last resort to life-threatening infections? |
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Definition
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Term
| What drug is BACTERIOCIDAL, mainly used against G- anaerobes, IRREVERSIBLE binding to 30S, SYNERGISTIC with b-lactam drugs, and can be used to target eukaryotic ribosomes? |
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Definition
| Aminoglycosides (drug names usually end in -mycin or -micin) |
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Term
| What are the 3 ways aminoglycosides work against bacteria? |
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Definition
-blocks initiation of protein synthesis
-blocks further translation and elicits premature termination
-incorporation of incorrect AA |
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Term
| Is Ticarcillin or Tobramycin good to give as a bolus (given a large amount above the MIC)? |
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Definition
Tobramycin (aminoglycoside)
ticarcillin (penicillin) is good to give a smaller dose a few times a day because there is no increased bacteria killing above MIC |
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Term
| What drug is a newer antibiotic that inhibits formation of 703 (keeps 30S and 50S from coming together), good for G+ but used as last resort drug to keep bacteria sensitive? |
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Definition
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Term
| Why characteristic make it so difficult to treat TB? |
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Definition
Mycobacterial cell surface is different from G+ or G-
-Can persist as an intracellular pathogen
-Slow growing
-Can lie dormant
-acid fast, cell wall with mycolic acids |
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Term
| What are the approved antimycobacterials for TB? |
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Definition
Fluroquinolones (inhibit DNA syn and target topoisomerase)
Rifomycin (inhibit RNA synthesis)
Streptomycin and Macrolides (inhibit protein synthesis)
other drugs inhibit mycolic acid synthesis, cell wall synthesis, cell membrane synthesis |
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Term
How would you want to treat TB?
Are the first line of drugs (bacteriostatic or bactericidal) |
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Definition
You must use drug combinations to prevent the development of resistance over 6mo-2 years because they're slow growing
use isoniazid, rifampin, pyrazinamide = bactericidal |
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