Term
| Drugs that inhibit bacterial protein synthesis typically target: |
|
Definition
| components of the bacterial ribosome |
|
|
Term
| How does selective toxicity result (with respect to drugs that inhibit protein synthesis)? |
|
Definition
| differences between bacterial & human ribosomes |
|
|
Term
| The two steps of protein synthesis that are targeted by antibacterials are: |
|
Definition
|
|
Term
| Initiation during protein synthesis involves: |
|
Definition
| formation of the ribosomal (translational) comples |
|
|
Term
| Elongation during protein synthesis involves: |
|
Definition
| entry of charged tRNA, peptide bond formation & translocation of the translational complex |
|
|
Term
| Most drugs that inhibit bacterial protein synthesis act on this step: |
|
Definition
|
|
Term
| Tetracyclines have how many rings? |
|
Definition
|
|
Term
| What does pass now/ pass later mean for SMS students? |
|
Definition
| don't stress-- you'll do great! |
|
|
Term
| What is the target of tetracyclines? |
|
Definition
|
|
Term
| How do tetracyclins work? |
|
Definition
| inhibit tRNA entry into the translational complex, blocking up the elongation step |
|
|
Term
| Tetracyclins inhibit which step of protein synthesis? |
|
Definition
|
|
Term
| Tetracylines are effective against: |
|
Definition
| bacteriostatic against Gram + and negatives, anaerobes, Mycoplasma spp. & Rickettsia spp. |
|
|
Term
| Tetracyclines are used to treat: |
|
Definition
mycoplasma pneumoniae, H. pylori, Rickettsiae spp., Chlamydiae spp. infections
also used for acne |
|
|
Term
| This drug is sometimes used to treat acne: |
|
Definition
|
|
Term
| Resistance to tetracyclines are usually due to: |
|
Definition
action of efflux pumps (plasmid-based)
variation fo these pumps --> variation in resistance patterns |
|
|
Term
| Adverse effects of tetracyclines include: |
|
Definition
GI disturbances -> N/V
superinfections with C. albicans, S. aureus, & C. dificile
discoloration & dysplasia of teeth & bone (don't give to kids <10 y/o)
hepatic & renal toxicity
photosensitivity |
|
|
Term
| Tetracyclines' oral bioavailability: |
|
Definition
|
|
Term
| Tetracyclines are chlated by cations such as: |
|
Definition
|
|
Term
Are tetracyclines recommended during pregnancy?
Why/ why not? |
|
Definition
| No, they can cross the placenta |
|
|
Term
| Glycylcyclin (Tigecycline) has what structural feature to preven extrusion by efflux pumps? |
|
Definition
|
|
Term
| Glycylcycline (Tigecycline) is active in vitro against: |
|
Definition
VRE, MRSA, & PRSP
also active against some multi-drug resistant Gram negatives |
|
|
Term
| Glycylcycline (Tigecycline) is used for: |
|
Definition
complex skin & intra-abdominal infections
use against multi-drug resistant bugs needs more evaluation |
|
|
Term
|
Definition
|
|
Term
| Chloramphenicol inhibits: |
|
Definition
| peptide bond formation & blocks elongation of growing peptide chains |
|
|
Term
| Chloramphenicol is bacteriostatic against: |
|
Definition
| Gram + and -, aerobes, anaerobes, Rickettsiae |
|
|
Term
| Chloramphenicol is bactericidal against: |
|
Definition
|
|
Term
| Chloramphenicol is used to treat: |
|
Definition
serious infections with Salmonella typhi, Bacteroides, and VRE
used for a broader range of severe infections (eg, meningitis) in patients allergic to penicillins |
|
|
Term
| A patient has a severe infections (eg, meningitis) and is allergic to penicillins. Treatment could be: |
|
Definition
|
|
Term
| Resistance to chloramphenicol is due to: |
|
Definition
| enzymatic acetylation of the drug (plasmid based) |
|
|
Term
| Chloramphenicol toxicity includes: |
|
Definition
GI disturbances --> N/V
superinfections with C. albicans
bone marrow suppression--> anemia & aplasia
gray baby syndrome (flaccidity, hypotension, hypothermia, & gray skin color) |
|
|
Term
| Chloramphenicol has good/bad oral bioavailability? |
|
Definition
|
|
Term
| Chloramphenicol tissue distribution: |
|
Definition
|
|
Term
| Chloramphenicol is inactivated by: |
|
Definition
| hepatic glucuronyl transferase |
|
|
Term
| Gray baby syndrome is caused by |
|
Definition
| use of chloramphenicol in some children |
|
|
Term
| Gentamycin, Tobramycin, Amikacin, Streptomycin are examples of: |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Aminoglycoside binding inhibits: |
|
Definition
| translation intiation--> misreading during protein synthesis & inhibits peptide elongation |
|
|
Term
| Aminoglycosides are bactericidal towards: |
|
Definition
| aerobic Gram - enteric bacteria |
|
|
Term
| Aminoglycosides exhibit which type of killing? |
|
Definition
|
|
Term
| Do aminoglycosides have a PAE? |
|
Definition
|
|
Term
| Aminoglycosides are used to treat: |
|
Definition
| serious Gram - infections, such as sepsis & pneumonia, enterococcal endocarditis (given with a B-lactam for synergistic effect), and TB |
|
|
Term
| aminoglycoside + B-lactam given to treat: |
|
Definition
| enterococal endocarditis (synergistic effect) |
|
|
Term
| What bugs are usually intrinsically resistant to aminoglycosides? |
|
Definition
| anaerobes (drug uptake is oxygen dependent) and to Gram + organisms (their thick cell walls are impermeable to aminoglycosides) |
|
|
Term
| Acquired resistance to aminoglycosides is due to: |
|
Definition
presence of transferases that attach acetate, phosphate, and adenylate gruops to these drugs (plasmid-based); amikacin is a poor substrate for these transferases
rarely, acquired resistance is due to:
target alteration, porin alteration |
|
|
Term
| Adverse effects of aminoglycosides include: |
|
Definition
ototoxicity (cochlear --> tinnitus, vestibular --> vertigo)
nephrotoxicity
*adverse effects reduced by once-daily dosing |
|
|
Term
| Aminoglycosides are administered: |
|
Definition
|
|
Term
| Do aminoglycosides enter the CNS? |
|
Definition
|
|
Term
| How are aminoglycosides eliminated? |
|
Definition
|
|
Term
| Why are aminoglycosides synergistic with penicillin? |
|
Definition
| disruption of the cell wall enhances uptake of aminoglycosides |
|
|
Term
| Erythromycin, Clarithromycin,& Azithromycin are examples of: |
|
Definition
|
|
Term
| Macrolides (erythromycin, clarithromycin, azithromycin) target: |
|
Definition
|
|
Term
|
Definition
| translocation, blocks elongation step |
|
|
Term
| Macrolides are bacteriostatic against: |
|
Definition
| Strep spp., Staph spp., Corynebacteria spp., Mycobacteria spp., Legionella spp., Neisseria spp., & some Rickettsia spp. |
|
|
Term
| macrolides are used to treat: |
|
Definition
community acquired pneumonia, corynebacterial & chlamydial infections
also used as a substitute for penicillin in allergic patients |
|
|
Term
| Resistance to macrolides is due to: |
|
Definition
efflux pumps (plasmid-based)
rRNA methylation (inducible plasmid-based) |
|
|
Term
| Bacteria resistant to one macrolide due to an efflux pump show: |
|
Definition
| cross-resistance to all other macrolides |
|
|
Term
|
Definition
Resistance to macrolides due to rRNA methylation
show cross-resistance to all macrolides, clindamycin & streptogramins
MLS= Macrolides, cLindamycin, Streptogramins |
|
|
Term
| adverse effects of macrolides include: |
|
Definition
GI disturbances --> N/V/D (less common with azithromycin)
hepatocellular toxicity |
|
|
Term
| All macrolides except azithromycin inhibit: |
|
Definition
|
|
Term
| How are macrolides administered? |
|
Definition
| orally, good oral bioavaialbility |
|
|
Term
| Macrolides distribute in the body: |
|
Definition
|
|
Term
| Do macrolides enter the CNS? |
|
Definition
|
|
Term
| Macrolides are eliminated: |
|
Definition
|
|
Term
| Azithromycin & dosing regimins: |
|
Definition
| has a long half life (5 days), so it can be given in simple dosing regimens |
|
|
Term
| Ketolides (Telithromycin) are derivatives of: |
|
Definition
|
|
Term
| Ketolides (Telithromycin) target: |
|
Definition
50S ribosome subunit
binding is 10x that of erythromycin |
|
|
Term
| Ketolides (Telithromycin) are bacteriostatic with an antibacterial spectrum similar to: |
|
Definition
|
|
Term
| Ketolides are/ are not active against bacterial strains that exhibit MLS resistance |
|
Definition
| are active against MLS resistant bacteria |
|
|
Term
| Ketolides are used to treat: |
|
Definition
| community acquired pneumonia, bronchitis, & sinusitis |
|
|
Term
| Adverse effects of ketolides include: |
|
Definition
prolonged QT interval, which can --> arrhythmias
liver toxicity
may be teratogenic |
|
|
Term
| Do Ketolides inhibit CYP34A? |
|
Definition
|
|
Term
|
Definition
| orally; good oral bioavailability |
|
|
Term
| Ketolides are metabolized by: |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Clindamycin is bacteriostatic against: |
|
Definition
| Strep spp., Staph. spp., & Bacteroides spp.; anaerobes |
|
|
Term
| Clindamycin is used to treat: |
|
Definition
infections with Bacteroides spp. & mixed aerobic/anaerobic infections OUTside the CNS
used as prophylaxis in patients pre-disposed to bacterial endocarditis & who are allergic to penicillins |
|
|
Term
| A patient is pre-disposed to bacterial endocarditis and is allergic to penicillins. Prophylactially, we can give: |
|
Definition
|
|
Term
| What organisms are intrinsically resistant to clindamycin? |
|
Definition
| Gram - (impermeable to the drug) |
|
|
Term
| Resistance to clindamycin is usually due to: |
|
Definition
| ribosomal RNA methylation (MLS resistance) |
|
|
Term
| Adverse effects of clindamycin include: |
|
Definition
| GI disturbances --> N/V/D & entercolitis due to C. difficile |
|
|
Term
| Does clindamycin enter the CNS? |
|
Definition
|
|
Term
| Clindamycin's oral bioavailability: |
|
Definition
|
|
Term
| Clindamycin is metabolized: |
|
Definition
|
|
Term
| Clindamycin is eliminated: |
|
Definition
|
|
Term
| Quinupristin/Dalfopristin are examples of: |
|
Definition
|
|
Term
| Quinupristin/Dalfopristin are always given in what ratio? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Streptogramins are bactericidal against: |
|
Definition
| Strep, Staph, Enterococcus faesium; Enterococcus fecalis is intrinsically resistant due to its production of an efflux pump |
|
|
Term
|
Definition
| Vancomycin-Resistant Enterococcus |
|
|
Term
True/false:
Streptogramins can be used to treat VRE |
|
Definition
|
|
Term
| Resistance to streptogramins is usually due to: |
|
Definition
| ribosomal methylation (MLS resistance) |
|
|
Term
| Adverse effects of streptogramins: |
|
Definition
| thrombophlebitis @ IV infusion site |
|
|
Term
| Streptogramins are metabolized by: |
|
Definition
|
|
Term
| Streptogramins are given by: |
|
Definition
|
|
Term
| Streptogramins inhibit CYP34A? |
|
Definition
|
|
Term
|
Definition
| RNA of 50S ribosomal subunit |
|
|
Term
| Oxazolidinones (Linezolid) blocks the formation of: |
|
Definition
|
|
Term
| Oxazolidinones (Linezolid) are bacteriostatic against: |
|
Definition
|
|
Term
| Oxazolidinones (Linezolid) are used to treat: |
|
Definition
|
|
Term
| Resistance to oxazolidinones (Linezolid) is due to: |
|
Definition
| mutation of ribosomal RNA binding site (seen in some enterococcal strains) |
|
|
Term
| Why hasn't cross resistance been observed with oxazolidinones (Linezolid)? |
|
Definition
| no other antibacterials have the same target (RNA of 50S ribosomal subunit) |
|
|
Term
| Adverse effects of Oxazolidinones (Linezolid): |
|
Definition
GI disturbances --> N/V
thrombocytopenia
rarely: neutropenia |
|
|
Term
| Oxazolidinones (Linezolid) are given by: |
|
Definition
| IV or oral administration |
|
|
Term
| Oxazolidinones (Linezolid) are eliminated by: |
|
Definition
|
|
Term
| Antimicrobial drugs that inhibit CYP34A & produce clinically important drug interactions: |
|
Definition
macrolides
ketolides
streptogramins
flurooquinolones
azole anti-fungal drugs
HIV protease inhibitors |
|
|
