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67 Cards in this Set
- Front
- Back
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what is an antibiotic? |
-a substance, produced by a microorganism, with the capacity to kill or inhibit growth of other organisms |
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what is an antimicrobial? |
- a substance which negatively effects microorganisms -also synthetic compounds |
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what does a bacteriostatic do? |
-inhibits microbial growth |
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what does a bacteriocidal do? |
-kills the organism |
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if two antimicrobials are used and there is no effect what is it called? |
- indifference |
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If combined antimicrobial agents are combined or added and give an effect of the drug it is considered what? |
-additive |
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the effect is much greater than using one antimicrobial over another than using combined single effects |
-synergistic |
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antagonistic |
-one drug counteracts the other |
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what is the main protective section of the cell wall? |
-peptidoglycan |
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what does the cell wall synthesis depend on? |
-specific integral enzymes |
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what will structurally/ functionally destroy bacterial cell walls? |
-inactivating or interfering with the integral enzymes |
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peptidoglycan |
-thick outer layer in gram positive -thin inner layer in gram negative -cell wall active antibiotics will be most effective against gram positive |
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what accounts for a large number of common antibacterial agents? |
- B lactam antibiotics |
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what is B-lactam's antibacterial activity based on? |
- B lactum ring structure |
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What do B-lactams bind to? |
-transpeptidase enzymes |
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Once B-lactams bind to transpeptidase enzymes what do they prevent them from doing? |
-prevents them from forming peptide bonds during peptidoglycan synthesis |
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because of the activity of transpeptidase enzymes what are they commonly referred to? |
-penicillin binding proteins (PBPs) |
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Penicillin's |
-are highly effective with low toxicity |
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Penicillin G |
-inactivated by gastric acid -given as a intravenous drug |
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Penicillin V |
-more resistant to acid -preferred by oral form |
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what have some penicillin's been combined with? |
- B lactamase inhibitors -clavulanic acid sulbactam |
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what do these B-lactamase inhibitors do? |
-can irreversibly bind and inactivate susceptible B-lactamases, permitting the companion drug to disrupt cell wall synthesis |
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Cephalosporins |
-B lactam antibiotics originally isolated from the mold cephalosporin |
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how do cephalosporins differ from penicillin? |
- have a wider antibacterial spectrum -resistant to many B-lactamases -have generations |
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carbapenems |
-active against virtually all groups of organisms |
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monobactams (narrow spectrum) |
-active against only aerobic, gram negative bacteria -not widely used |
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Vancomycin (glycopeptides) |
-originally obtained from streptomyces -large molecule
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how does vancomycin disrupt cell wall peptidoglycan synthesis? |
-by interfering with the formation of bridges between the peptidoglycan chains |
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what is vancomycin primarily used for? |
-against gram positive bacteria -to large to pass through LPS porins to reach peptidoglycan layer in gram negative bacteria |
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inhibiting protein synthesis |
-agents bind to either the 50s or 30s ribosomal subunit blocking translation |
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binding to a ribosome can be |
reversible-inhibition of protein synthesis or irreversible- death |
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aminoglycosides |
-irreversibly bind to 30s ribosomal subunit |
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the binding of aminoglycosides of what two effects? |
-misreading of the mRNA resulting in the production of aberrant proteins -interruption of protein synthesis by causing premature release of the ribosome from the mRNA -used against gram negative rods |
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what are the most commonly used aminoglycosides? |
-amikacin -gentamicin -tobramycin |
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tetracyclines |
-reversibly bind to the 30s subunit |
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what are tetracyclines effective against? |
-chlamydia, mycoplasma, rickettsia, & selected gram postive and gram negative bacteria |
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what are the most common tetracyclines? |
-tetracycline -doxycycline -minocycline |
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Macrolides |
-bind reversibly to the 50s subunit |
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what are macrolides effective on? |
- gram positives |
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what are the most common macrolides? |
-erythromycin -azithromycin -clarithromycin |
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What affects nucleic acid synthesis? |
-quinolones -Rifampin -metronidazole |
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Quinolones |
-inhibit bacterial DNA in topoisomerase type II (gyrase): gyrase-A subunit is primary target in gram negative bacteria -inhibits topoisomerase IV: primary target in gram positive bacteria |
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what does nalidixic acid inhibit? |
-gyrase |
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what is nalidixic acid used to treat? |
-urinary tract infections of gram negative bacteria |
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the drug resistance of nalidixic acid lead to the development of what? |
-fluorinated quinolones |
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what fluorinated quinolones are used against gram negative aerobes? |
-ciprofloxacin, norfloxacin |
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what fluorinated quinolones are used against gram positive aerobes? |
-levifloxacin & moxifloxacin (streptococcus pneumonia) |
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What does Rifampin bind to and inhibit? |
-binds to RNA polymerase & inhibits the initiation of RNA synthesis |
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Rifampin |
-bactericidal for mycobacterium -very active against gram positive cocci
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Metronnidazole |
-makes DNA unstable -used against anaerobes |
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antimetabolites primarily target what? |
-the folate synthesis pathway
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folates are essential for what? |
-for the synthesis of many molecules in bacteria, especially DNA- synthesized from p aminobenzoic acid (p ABA) |
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sulfnoamides |
-structure is similar to p-ABA, so they compete for enzyme docking |
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Trimethoprim |
-inhibits enzyme used for folate synthesis |
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these two antimetabolites are usually used together to produce what effect? |
-a synergistic effect |
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Bacitracin |
-was isolated from Bacillus too toxic to be used internally -skin only -inhibits transport of peptidoglycan monomers across the plasma membrane -mainly for gram positive |
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polymyxins |
-insert into bacterial membranes & interact w/ LPS & phospholipids, altering permeability -used externally for gram negative rods |
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how can resistance to antimicrobial agents be acquired? |
-can be acquired from other microbes (via transfer of DNA), or initiated by a mutation in the bacterial DNA |
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What are mechanisms of resistance? |
-inhibiting uptake of drug -increased excretion of drug- efflux pump -structural or functional modification of the drug target -inactivating the drug- enzymes |
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how can bacteria become resistant to B-lactam antibiotics? (3 ways) |
-prevention of the interaction between the antibiotic & the target PBP -modification of the binding of the antibiotic to the PBP -hydrolysis of the antibiotic by B lactamases |
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extended-spectrum B- lactamases (ESBLs) |
- single point mutations in the genes encoding B lactamases in some gram negative rods cause activity against all penicillins & cephalosporins |
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B-lactamases are in the same family as... |
- PBP |
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Vancomycin susceptible |
-targets growing peptidoglycan chain |
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Vancomycin Resistant strain |
-contains genes that code for altered peptidoglycan synthesis |
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Nitrocefin |
-same structure as B lactam antibiotic, but turns pink when treated with B lactamase -rapid test method |
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Intrinsic Resistance |
-resulting from normal genetic, structural, or physiologic state of the microorganism |
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Efflux |
-natural occurring intrinsic resistance of bacteria -in gram pos & gram neg bacteria -function as transporter proteins in the cell membrane to eliminate toxic substances from interior of cell to external environment - |
