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33 Cards in this Set
- Front
- Back
This substance, a component of folic acid, antagonizes the action of sulfonamides.
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p-aminobenzoic acid (PABA)
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The addition of what antibiotic to dihydropteroic acid inhibits the synthesis of folic acid?
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sulfanilamide
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When substance A is added, proportionally more of substance B is required to counteract its action. This is an example of what?
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competitive inhibition
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Why are body cells unaffected by sulfonamides?
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Because they require preformed folic acid.
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Sulfonamides inhibit the SYNTHESIS of folic acid, but not its UTILIZATION. So why aren't bacteria able to use other sources of preformed folic acid?
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Many bacteria that make folic acid lack a system for the uptake of preformed folic acid and cannot benefit from its presence in the environment.
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When sulfanilamide is added, why must bacteria progress through 2-4 generations before growth is inhibited?
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Each bacterium contains enough preformed folic acid to meet the demands of up to 16 daughter cells.
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Name a few important examples when bactericidal agents are preferred to bacteriostatic ones.
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bacterial endocarditis, bacterial meningitis and infections in patients with low numbers of circulating neutrophils
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Give an example when a bacteriostatic drug might be preferable to a bactericidal one.
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Infection with clostridium perfringes (agent of gas gangrene) or other toxin producing bacteria
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These antibiotics are taken up poorly by bacteria under anaerobic conditions and are thus ineffective against anaerobes.
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aminoglycosides
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This drug is concentrated in the urine and is effective in many cases of uncomplicated urinary tract infections.
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nitrofurantoin
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This drug blocks the function rather than the synthesis of folic acid.
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trimethoprim
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What is the mechanism of action for trimethoprim?
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It inhibits the enzyme dihydrofolate reductase, which catalyzes the reduction of dihydrofolate to tetrahydrofolate. The drug can be used against bacteria and protozoa at concentrations that do not harm humans.
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Three steps of action for antimicrobial drugs:
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1. associate with the bacteria and penetrate their evelope
2. be transported to an intracellular site of action 3. must bind to their specific biochemical target |
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List five clinically relevant mechanisms of resistance:
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1. synthesis of enzymes that break down the drug molecule
2. chemical modification of the drug that interferes with its function 3. prevention of access to the target site by inhibiting uptake 4. prevention of access to the target site by increasing export of the drug from the microbial cell 5. modification of the target site |
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what is the main difference between 1st and 2nd or 3rd generation cephalosporins
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the addition of new side chains to extend the spectrum of activity to organisms that were resistant and to increase penetration into the CNS
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List the 4 steps of bactericidal action of the B-lactams:
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1. association with the bacteria
2. penetration through the outer membrane and the periplasmic space (in gram neg) 3. interaction with penicillin-binding proteins on the cytoplasmic membrane 4. activation of an autolysin that degrades the cell wall murein |
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Two major categories of B-lactamases:
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penicillinases and the cephalosporinases
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Where are the B-lactamases produced in gram (+) bacteria?
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extracellularly
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Where are the B-lactamases found in gram (-) bacteria?
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in the periplasmic space or bound to the inner membrane
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In gram (-) bacteria, B-lactams must be able to pass through outer membrane porins to make contact with what?
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penicillin-binding proteins (PBPs)
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Altering the PBPs so they no longer bind to B-lactams has been an important resistance mechanism for what two bacteria?
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PCN resistant streptococcus pneumoniae and methycillin resistant staphylococcus aureus
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This drug inhibits peptidoglycan chain elongation by binding to the D-ala-D-ala terminal peptides on the precursor
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vancomycin
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Mechanism of vancomycin resistance
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the production of precursors with D-lactate in the position of the terminal D-ala, thereby blocking the binding of vancomycin
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These antibiotics act by inhibiting the action of bacterial topoisomerases, including DNA gyrase (in gram pos) and topoisomerase IV (in gram neg)
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quinolones
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Three steps in the mechanism of action of aminoglycosides (an antiribosomal antibiotic)
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1. penetration of the outer membrane of gram (-)
2. association with a two-stage active transport system in the cell membrane (irreversible) 3. binding to the 30S ribosome subunit to inhibit protein synthesis, primarily at or near the initiation step, and to increase "miscoding" by the ribosomes and the production of "nonsense proteins." |
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Most common mechanism in clinically important resistance of aminoglycosides:
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modifying enzymes that modify these antibiotics by the addition of acetyl, adenyl, or phosphoryl groups
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erythromycin, clindamycin, azithromycin and clarithromycin are examples of what kind of antibiotics?
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macrolide antibiotics
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elimination of antibiotics from bacterial cells is an example of what type of resistance?
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efflux pumps
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Linezolid, and entirely synthetic antibiotic is an example of what class of drugs?
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oxazolidinones
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These drugs bind more avidly to ergosterol in the membranes of fungi than to cholesterol in the membranes of higher eukaryotes.
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polyenes
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This group of anti-fungal drugs targets cytochrome P450 demethylase, which is involved in sterol synthesis.
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imidazoles
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This group of anti-fungals inhibits B-glucan, a component of the fungal cell wall.
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echinocandins
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what is transpeptidase?
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You might know it as penicillin binding protein (PBP). It is the enzyme that catalyzes the formation of the peptidoglycan linkages in the bacterial cell wall.
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