Term
| What group of penicillins do Aq Pen G, Benzathine Penicillin, Procaine Penicillin, and Penicillin VK belong to? |
|
Definition
|
|
Term
| What group of penicillins do Nafcillin, Oxacillin, and Dicloxacillin belong to? |
|
Definition
| Penicillinase-resistant penicillins |
|
|
Term
| What group of penicillins do Ampicillin and Amoxicillin belong to? |
|
Definition
|
|
Term
| What group of penicillins does Ticarcillin belong to? |
|
Definition
|
|
Term
| What group of penicillins does Piperacillin belong to? |
|
Definition
|
|
Term
| What are three B-lactamase inhibitor combinations? |
|
Definition
Ampicillin-Sulbactam (Unasyn)
Amoxicillin-Clavulanate (Augmentin)
Piperacillin-Tazobactam (Zosyn) |
|
|
Term
| What are some general characteristics of B lactams? |
|
Definition
1. Same MOA - inhibit cell wall synthesis
2. Same MOR - B-lactamase degradation, PBP alteration, decreased penetration
3. Bactericidal in a time-dependent manner
4. short elimination half-life of <2 hours
5. Primarily eliminated unchanged by the kidneys
6. Cross-allergenicity |
|
|
Term
| What bacteria species the exception to B-lactams being bactericidal? What drug is best to use? |
|
Definition
Enterococcus spp.
Ampicillin is drug of choice and is bacteriostatic |
|
|
Term
| What B-lactams are not eliminated by the kidneys? |
|
Definition
| nafcillin, oxacillin, ceftriaxone, cefoperazone |
|
|
Term
| What B-lactam does not display cross-allergenicity? |
|
Definition
|
|
Term
| What molecular characteristics do all penicillins share? |
|
Definition
| B-lactam ring, thiazolidine ring and an R site where we can add side chains |
|
|
Term
| What are PBPs and when are they expressed? |
|
Definition
PBPs = Penicillin binding proteins found on the bacterial cell walls
They are only expressed during cell division!! |
|
|
Term
| What does inhibition of PBPs lead to? |
|
Definition
| Inhibition of the final transpeptidation step of peptidoglycan synthesis |
|
|
Term
| What is the most important and most common mechanism of resistance to penicillins? |
|
Definition
| production of B-lactamase enzymes that hydrolyze the B-lactam ring, inactivating the antibiotic |
|
|
Term
| Where are B-lactams found in gram positive cells? |
|
Definition
|
|
Term
| Where are B-lactams found in gram negative cells? |
|
Definition
| periplasm (porins must let the abx in) |
|
|
Term
| How does MRSA resist penicillin? |
|
Definition
| changes the PBPs leading to decreased affinity for the binding site |
|
|
Term
| What is one mechanism of resistance to penicillins that gram negative bacteria have that gram positive do not? |
|
Definition
| alteration of outer membrane porin proteins leading to decreased penetration |
|
|
Term
| What is the spectrum of activity (SOA) for Natural Penicillins? |
|
Definition
Gram + = Group strep, Viridans Strep
Gram - = Neisseria spp.
Anaerobes = Clostridum spp.
Other = Treponema pallidum (SYPHILIS) |
|
|
Term
| Why were Penicillinase-Resistant Penicillins developed? |
|
Definition
| to respond to the emergence of penicillinase-producing Staphylococcus |
|
|
Term
| What is the SOA for Penicillinase-Resistant Penicillins? |
|
Definition
Gram + = MSSA
(essentially it is better for S aureus but worse for everything else) |
|
|
Term
| Why were Aminopenicillins developed? |
|
Definition
| to respond to the need for agents with gram-negative activity |
|
|
Term
| What is the SOA for Aminopenicillins? |
|
Definition
Gram + = Enterococcus spp., Listeria monocytogenes
Gram - = Proteus mirabilis, some E. coli, Salmonella, Shigella, BL-H. influenzae |
|
|
Term
| Why were Carboxypenicillins developed? |
|
Definition
| to respond to the need for agents with enhanced activity against gram-negative bacteria |
|
|
Term
| What is the SOA for Carboxypenicillins? |
|
Definition
| Gram - = Pseudomonas aeruginosa |
|
|
Term
| Why were Ureidopenicillins developed? |
|
Definition
| to respond to the need for agents with even more enhanced activity against gram-negative bacteria |
|
|
Term
| What is the SOA for Ureidopenicillins? |
|
Definition
Gram - = Enterobacter spp, Pseudomonas aeruginosa, Serratia marcescens, some Klebsiella spp.
-fairly good activity against anaerobes |
|
|
Term
| What is the most active Penicillin against P. Aeruginosa? |
|
Definition
|
|
Term
| Why were B-lactamase Inhibitor Combinations developed? |
|
Definition
| to enhance activity of the penicillins against B-lactamase-producing bacteria |
|
|
Term
| What is the SOA for B-lactamase Inhibitor Combinations? |
|
Definition
Gram + = S. aureus (not MRSA)
Gram - = H. influenzae, Moraxella caterrhalis
Anaerobes = Bacteroides spp. |
|
|
Term
| What penicillin is used to treat Bacteroides Fragilis? |
|
Definition
| B-Lactamase Inhibitor Combos |
|
|
Term
| How do the penicillins distribute to the CSF? |
|
Definition
| adequate CSF concentrations only achieved in the presence of inflamed meninges with high-dose parenteral administration |
|
|
Term
| How well do the penicillins distribute body fluids and tissues? |
|
Definition
| Penicillins are widely distributed into body tissues and fluids including pleural fluid, synovial fluid, bone, bile, placenta, and pericardial fluid, but do NOT penetrate the eye or prostate. The variation in distribution of various penicillins depends on their molecular configuration and protein binding. |
|
|
Term
| How is nafcillin eliminated from the body? |
|
Definition
|
|
Term
| How is oxacillin eliminated from the body? |
|
Definition
|
|
Term
| What penicillins are removed by hemodialysis? |
|
Definition
| All except nafcillin and oxacillin |
|
|
Term
| Which penicillins should be used with caution in patients with CHF or renal failure due to the sodium load associated with their parenteral formulations? |
|
Definition
Ticarcillin*
Carbenicillin
Sodium Pen G
Piperacillin |
|
|
Term
| Which parental penicillin agent has the most mEq of sodium per gram? |
|
Definition
|
|
Term
| What are the major adverse effects associated with penicillin abx? |
|
Definition
| hypersensitivity - severe anaphylaxis and death, cross-reactivity exists among all penicillins and even some other B-lactams, seizures, leukopenia, neutropenia, thrombocytopenia, GI problems, interstitial nephritis, phelbitis, hypokalemia, Na overload |
|
|
Term
| Which penicillins are most likely to cause interstitial nephritis? |
|
Definition
| Methicillin and Nafcillin |
|
|
Term
| What are the main clinical uses of natural penicillins? |
|
Definition
| PSSP, infections due to streptococci, Neisseria meningitis, syphilis, C. perfringens, C. tetani |
|
|
Term
| What are the main clinical uses of Pencillinase-Resistant Penicillins? |
|
Definition
|
|
Term
| What are the main clinical uses of Aminopenicillins? |
|
Definition
| Enterococcal infections, Listeria monocytogenes |
|
|
Term
| What are the main clinical uses of Carboxypenicillins and Ureidopenicillins? |
|
Definition
| hospital-acquired infections, infections due to P. aeruginosa (esp Piperacillin) |
|
|
Term
| What are the main clinical uses of B-lactamase inhibitor combos? |
|
Definition
| polymicrobial infections, empiric therapy for febrile neutropenia or hospital-acquired infections |
|
|
Term
| What are the 4 classes of drugs in B-lactams? |
|
Definition
Pencillins
Cephalosporins
Carbapenems
Monobactams |
|
|
Term
| Which bacteria produce B-lactamase? |
|
Definition
Gram + = PRSA
Gram - = Kleb pneumoniae, Haemophilus influenze, M. catarrhalis, E coli, Enterobacter, Neisseria gonnorrhoeae
Anaerobes = Bacteroides fragilis |
|
|
Term
| Which generation of Cephalosporins is most stable against B-lactamase enzymes? |
|
Definition
|
|
Term
| Which bacteria produce B-lactamase after induction by certain cephalosporins? |
|
Definition
|
|
Term
| What are bacterial resistance mechanisms to the cephalosporins? |
|
Definition
| Alteration of PBPs leading to decreased binding affinity (MRSA, PRSP) and alteration of outer membrane leading to decreased penetration to the PBPs |
|
|
Term
| What two factors are the "generations" of Cephalosporins based on? |
|
Definition
| antimicrobial activity and resistance to B-lactamase enzymes |
|
|
Term
| What do the First Generation Cephalosporins (Cefazolin and Cephalexin) have activity against? |
|
Definition
| Gram-positive aerobes (MSSA, PSSP, group Strep, Viridans Strep) and Gram-negatives PEK (Proteus mirabilis, E. coli, Klebsiella pneumoniae) |
|
|
Term
| What do the Second Generation Cephalosporins (Cefuroxime, Cefprozil, Cefoxitin, Cefotetan) have activity against? |
|
Definition
| Gram-positive aerobes (not as good as 1G) and Gram-negatives HENPEK (Haemophilus influenzae, some Enterobacter spp., Neisseria spp., P. mirabilis, E. coli, K. pneumoniae) and anaerobes |
|
|
Term
| Which second generation is used the most in surgery? |
|
Definition
|
|
Term
| Which Cephalosporins have activity against anaerobes (Bacteroides)?** |
|
Definition
|
|
Term
| What do the Third Generation Cephalosporins (Ceftriaxone, Ceftazidime, Cefpodoxime) have activity against? |
|
Definition
| Gram-positive aerobes (not as good as 1G or 2G) and Gram-negatives HENPECKSSS (Haemophilus influenzae, some Enterobacter spp., Neisseria spp., P. mirabilis, E. coli, Citrobacter sp., K. pneumoniae, Serratia marcescens, Salmonella sp., Shigella sp.) and P. AERUGINOSA |
|
|
Term
| Which 3G Cephalosporins can treat P. aeruginosa?** |
|
Definition
| Ceftazidime and Cefpodoxime |
|
|
Term
| Which 3G Cephalosporin is used for uncomplicated gonnorrhea? |
|
Definition
|
|
Term
| Which 3G Cephalosporin is used the most frequently? |
|
Definition
|
|
Term
| Which 3G Cephalosporin should be used in meningitis if pseudomonas is present or suspected? |
|
Definition
|
|
Term
| Which 3G Cephalosporin can be an inducer of B-lactamase? |
|
Definition
|
|
Term
| Which 3G Cephalosporin has the longest half life? |
|
Definition
|
|
Term
| Which 3G Cephalosporins do not have renal elimination? |
|
Definition
Cefotaxime - biliary elimination
Ceftriaxone - hepatic elimination |
|
|
Term
| What does the Fourth Generation Cephalosporin (Cefepime) have activity against? |
|
Definition
| similar gram + and gram - killing to 3G, kills P. aeruginosa, also covers B-lactamase producing Enterobacter spp. |
|
|
Term
| What does the Fifth Generation Cephalosporin (Ceftaroline) have activity against? |
|
Definition
| Community acquired bacterial pneumonia, SSSI; basic MRSA (not bacteremia) *has extended activity compared to other Cephalosporins |
|
|
Term
| What are some main bacteria that Cephalosporins do NOT have activity against? |
|
Definition
MRSA in the BLOOD
Enterococcus spp.
Listeria monocytogenes
Stenotrophomonas maltophilia
C. diff
atypical bacteria including Legionella |
|
|
Term
| Which Cephalosporins can achieve sufficent CSF concentrations? |
|
Definition
parenteral cefuroxime
3G and 4G |
|
|
Term
| When are Cephalosporins contraindicated? |
|
Definition
| if the pt has a severe allergy to penicillin; IgE mediated reaction; iv calcium |
|
|
Term
| What are some adverse effects of Cephalosporins? |
|
Definition
| hypersensitivity (5% overall); MTT side chain can cause hypoprothrombinemia; leukopenia, thrombocytopenia; if someone has been on Cephs for a while they are also susceptible to C diff. |
|
|
Term
| What are the 4 Carbapenems? |
|
Definition
imipenem
meropenem
ertapenem
doripenem |
|
|
Term
| How do Carbapenems differ from Cephalosporins? |
|
Definition
| Carbapenems have extended spectrum of antimicrobial activity beyond Cephalosporins.. they are the MOST BROAD SPECTRUM agents available. They also have activity against gram + and gram - aerobes (even B-lactamase producing strains) AND anaerobes |
|
|
Term
| How does the MOA of Carbapenems differ from Penicillins and Cephalosporins? |
|
Definition
| They primarily bind PBP-2 (not PBP) but the rest is the same |
|
|
Term
| What bacteria are NOT covered by Carbapenems?** |
|
Definition
| MRSA, PRSP, VRE, coag-neg staph, C diff, atypical bacteria, S. maltophilia |
|
|
Term
| Which Carbapenems have the best activity against Gram-positive aerobes? |
|
Definition
imipenem and doripenem
"New MDs Prove ID" |
|
|
Term
| Which Carbapenems have the best activity against Gram-negative aerobes? |
|
Definition
meropenem and doripenem
"New MDs Prove ID" |
|
|
Term
| Which Carbapenem does NOT have activity against P. aeruginosa? |
|
Definition
|
|
Term
| What Gram-positive anaerobes do Carbapenems have activity against? |
|
Definition
| Peptococcus spp, Peptostreptococcus spp., Veillonella, Clostridium spp. (NOT C diff) |
|
|
Term
| What Gram-negative anaerobes do Carbapenems have activity against? |
|
Definition
| Bacteriodes spp*, Fusobacterium, Prevotella spp. |
|
|
Term
| How do the Carbapenems distribute in the body? CSF? |
|
Definition
| widely distributed into body tissues and fluids, Meropenem is the best for CSF penetration |
|
|
Term
| Which Carbapenem can decrease the seizure threshold? |
|
Definition
|
|
Term
| How are Carbapenems eliminated? |
|
Definition
|
|
Term
| What happens to Imipenem in the kidney?* |
|
Definition
| It undergoes a hydrolysis reaction by a dihydropeptidase enzyme in the renal brush border to a nephrotoxic metabolite |
|
|
Term
| How do we make Imipenem last longer in the body?* |
|
Definition
| administer it with Cilastatin, which is a DHP inhibitor |
|
|
Term
| Which Carbapenem has the longest half life?* |
|
Definition
|
|
Term
| What are Carbapenems used for clinically? |
|
Definition
| Empiric therapy for hospital acquired infections; polymicrobial infections; infections due to B-lactamase-producing organisms (SPICE, SPACE, others); if Pseudomonas is unknown or suspected |
|
|
Term
| What are the greatest risk factors to be aware of when using Carbapenems? |
|
Definition
| SEIZURES (especially with pre-existing CNS disorder, high doses, and renal insufficiency) |
|
|
Term
| What is the only monobactam currently available? |
|
Definition
|
|
Term
| How is the MOA of aztreonam different from the other B-lactams? |
|
Definition
| It inhibits cell wall synthesis by primarily binding PBP-3 |
|
|
Term
| What does Aztreonam have activity against? |
|
Definition
| ONLY Gram NEG aerobes (including P. aeruginosa) |
|
|
Term
| What is Aztreonam used for clinically? |
|
Definition
| UTI, resp tract infections, meningitis, bacteremia, skin and soft tissue infections, intraabdominal infections due to gram-neg aerobes |
|
|
Term
| What is different about Aztreonam compared to other B-lactams? |
|
Definition
| no cross-reactivity with penicillins, can be used in penicillin-allergic pts |
|
|
Term
| What was Vancomycin originally developed for? |
|
Definition
| to treat PCN resistant S aureus |
|
|
Term
| What was the first name for Vancomycin? |
|
Definition
|
|
Term
| What is Vancomycin used to treat? |
|
Definition
| Gram-positive organisms, MRSA, CNSt, C diff, PCN resistant gram-pos cocci (PRSP) |
|
|
Term
| What is the MOA for Vancomycin? |
|
Definition
| Cell wall synthesis inhibitor (at a different site than B-lactams); binds firmly to D-alanyl-D-alanine portion of cell wall precursors to prevent cross-linking and further elongation of peptidoglycan; very slow killer (couple to several days) |
|
|
Term
| When is it appropriate to give oral Vancomycin? |
|
Definition
|
|
Term
| What do you need to use to calculate Vanco dosing? Why? |
|
Definition
| TBW; Vancomycin distributes all over the body and can get wherever we need it |
|
|
Term
| How long does Vanco take to distribute from plasma into tissue compartment?* |
|
Definition
|
|
Term
| What does Vanco elimination half life depend on? |
|
Definition
| renal function (but it is NOT removed by hemodialysis) |
|
|
Term
| When should the peak conc be drawn for iv Vanco? |
|
Definition
| 60 minutes after the end of infusion (need to wait for it to be distributed) |
|
|
Term
| What is Vancomycin used for clinically? |
|
Definition
| mainly for MRSA (infection anywhere in the body); patients who have serious gram + infections and have a B-lactam (esp Pencillin) allergy; multidrug resistant (PRSP); surgical prophylaxis (esp in combination with aztreonam); moderate to sever C. diff colitis |
|
|
Term
| What are the pharmacokinetic characteristics of Vancomycin? |
|
Definition
| Time-dependent bactericidal activity; slowly kills bacteria (static against Enterococcus). Widely distributed – can treat almost any infection in the body, even the CSF with inflamed meninges. |
|
|
Term
| What are the adverse effects of Vancomycin? |
|
Definition
| Red-Man Syndrome, which is due to too fast a rate of infusion. Vanco needs to be infused over a minimum of 1 hour. The symptoms of flushing, pruritus, erythematous rash are due to histamine release. Vanco can also cause nephrotoxicity and ototoxicity– see it more now when Vanco is administered with another nephrotoxic/ototoxic agent like an aminoglycoside. |
|
|
Term
| What is the MOR to Vancomycin? |
|
Definition
| modifications of the D-ala-D-ala binding site. There are 3 phenotypes this binding site that change D-ala-D-ala. Also, a type of S. aureus called VISA (vanco intermediate S aureus) has thickened cell wall that Vancomycin cannot penetrate |
|
|
Term
| Why was Linezolid developed? |
|
Definition
| to respond to a need for antibiotics with activity against resistant Gram-positives (VRE, MRSA, VISA) |
|
|
Term
| What is the MOA of Linezolid? |
|
Definition
| inhibits protein synthesis at INITIATION. Linezolid binds to the 50S ribosomal subunit near the surface interface of the 30S subunit – causes inhibition of 70S initiation complex (unique binding site), which inhibits protein synthesis. |
|
|
Term
| What is the MOR to Linezolid? |
|
Definition
| alteration in ribosomal binding sites (rare) |
|
|
Term
| What is the SOA for Linezolid? |
|
Definition
| mostly against Gram + bacteria: MSSA, MRSA, VRSA, all streptococcus including PRSP, Enterococcus faecium and faecalis (including VRE), anaerobic gram + skin flora; atypical bacteria – mycobacteria |
|
|
Term
| What are the pharmacokinetic characteristics of Linezolid? |
|
Definition
| time-dependent bactericiostatic activity (only cidal vs S pneumo). Post-antibiotic effect for Gram +; 100% bioavailability -- do not need to adjust dose from iv to po. Readily distributes all over the body, good CSF penetration = 30% |
|
|
Term
| What are the major clinical uses of Linezolid? |
|
Definition
| reserved for serious/complicated infections caused by resistant gram-positive bacteria: VRE bacteremia, complicated SSSI, nosocomial pneumonia due to MRSA, other serious infections due to MRSA; good penetration for CNS so it can be used for VRE abscess in brain; (NOT used for UTI) |
|
|
Term
| What are the major adverse reactions from Linezolid? |
|
Definition
| Lactic acidosis; peripheral neuropathy (if pt is on for a long time, which is why Linezolid is not used for things like osteomyelitis or endocarditis that have to be treated for 6+ weeks); thrombocytopenia* or anemia > 2-4% (in only 10-14 days) |
|
|
Term
| What are the major drug interactions with Linezolid? |
|
Definition
| Serotonin Syndrome with SSRIs/MAOIs – hyperpyrexia, diarrhea, cognitive dysfunction, restlessness, seizures, coma |
|
|
Term
| What is the MOA of Daptomycin? |
|
Definition
| binds to bacterial membranes which leads to rapid depolarization of membrane potential causing inhibition of protein, DNA, and RNA synthesis |
|
|
Term
| What is the SOA for Daptomycin? |
|
Definition
| used for resistant gram positive bacteria like VRE, MRSA, VISA |
|
|
Term
| When should Daptomycin not be used? |
|
Definition
|
|
Term
| What are the pharmacokinetic characteristics of Daptomycin? |
|
Definition
| concentration-dependent bactericidal activity, readily distributes into well-perfused tissue except lungs |
|
|
Term
| What are the major clinical uses of Daptomycin? |
|
Definition
| reserved for serious/complicated infections caused by resistant bacteria, especially VRE |
|
|
Term
| What are the major adverse reactions from Daptomycin? |
|
Definition
| myopathy and CPK (creatinine phosphokinase) elevation (<2%)* (when you stop the Daptomycin they feel better within 24 hr), nausea, diarrhea, headache, rash |
|
|
Term
| What is the major drug interaction with Daptomycin? |
|
Definition
| HMG CoA-reductase inhibitors (statins) – may lead to increased incidence of myopathy |
|
|
Term
| What are four favorable characteristics of Fluoroquinolones? |
|
Definition
-broad spectrum of activity
-excellent oral bioavailability
-excellent tissue penetration
-long half-lives |
|
|
Term
| What is the biggest disadvantage of fluoroquinolones? |
|
Definition
| development of resistance |
|
|
Term
| What is the mechanism of action of the fluoroquinolones? |
|
Definition
| Ultimately they inhibit DNA synthesis causing cell death in one of two ways – inhibiting DNA Gyrase (Topoisomerase II), which normally removes excess poritive supercoiling in the DNA helix, and Topoisomerase IV, which is essential for separation of interlinked daughter DNA |
|
|
Term
| Which DNA synthesis enzyme is the primary target of fluoroquinolones in Gram-negative bacteria? |
|
Definition
|
|
Term
| Which DNA synthesis enzyme is the primary target of fluoroquinolones in Gram-positive bacteria? |
|
Definition
|
|
Term
| How do bacteria develop resistance to the fluoroquinolone antibiotics? |
|
Definition
Main = mutations in DNA gyrase and Topoisomerase IV which results in a decreased binding affinity and the abx will not work
Other mechanisms = the expression of an efflux pump, decreased porin expression, cross-resistance between FQs |
|
|
Term
| What is the older fluoroquinolone that is currently used? |
|
Definition
|
|
Term
| What are the newer fluoroquinolones that are currently used? |
|
Definition
| Levofloxacin and Moxifloxacin |
|
|
Term
| What is the SOA of Ciprofloxacin? |
|
Definition
| poor activity against gram + aerobes; excellent activity against gram - aerobes; atypical bacteria including Legionella, Chlamydia, Mycoplasma, Ureaplasma |
|
|
Term
| What is the SOA of Levofloxacin? |
|
Definition
| enhanced activity against gram + aerobes; excellent activity against gram - aerobes; atypical bacteria including Legionella, Chlamydia, Mycoplasma, Ureaplasma |
|
|
Term
| What is the SOA of Moxifloxacin? |
|
Definition
| enhanced activity against gram + aerobes; fair activity against gram - aerobes; anaerobes; atypical bacteria including Legionella, Chlamydia, Mycoplasma, Ureaplasma |
|
|
Term
| Which fluoroquinolones have the best activity against Staph aureus? |
|
Definition
|
|
Term
| Which fluoroquinolones have the best activity against Strep pneumoniae? |
|
Definition
|
|
Term
| Which fluoroquinolones have the best activity against P. aeruginosa? |
|
Definition
|
|
Term
| Which fluoroquinolone has the best activity against anaerobes? |
|
Definition
|
|
Term
| Which fluoroquinolones have the best activity against atypical bacteria? |
|
Definition
|
|
Term
| What type of pharmacokinetics of bacterial killing do fluoroquinolones have? |
|
Definition
concentration-dependent
AUC/MIC correlates with efficacy |
|
|
Term
| How long does the PAE last for Fluoroquinolones? |
|
Definition
2 hours for Gram-positive bacteria
2-4 hours for Gram-negative bacteria |
|
|
Term
| What is the oral bioavailability for fluoroquinolones? |
|
Definition
|
|
Term
| What is the tissue distribution of FQs? |
|
Definition
extensive - lung, SSSI, bone
urinary tract and prostate (cipro and levo) |
|
|
Term
| What is the CSF penetration of FQs? |
|
Definition
|
|
Term
| What is the dosing interval for FQs? |
|
Definition
|
|
Term
| What is the route of elimination for FQs? |
|
Definition
| kidneys except for Moxi which is the liver |
|
|
Term
| What are the main clinical uses of Ciprofloxacin? |
|
Definition
| Upper resp tract infections (sinusitis, AECB), nosocomial pneumonia, bacterial exacerbations in CF, cystitis, pyelonephritis, prostatitis |
|
|
Term
| What are the main clinical uses of Levofloxacin? |
|
Definition
| Upper resp tract infections (sinusitis, AECB), CA-pneumonia, nosocomial pneumonia, cystitis, pyelonephritis, prostatitis |
|
|
Term
| What are the main clinical uses of Moxifloxacin? |
|
Definition
| Upper resp tract infections (sinusitis, AECB), CA-pneumonia |
|
|
Term
| What are the major adverse effects associated with fluoroquinolone therapy? |
|
Definition
GI: nausea, vomiting, diarrhea, dyspepsia, C. diff colitis
CNS: headache, dizziness, insomnia, seizures(elderly)
Hepatotoxicity: not too much of a problem now but increase in proteins
Phototoxicity
Cardiac: prolongation of QT interval (worry about pts with an already prolonged QT interval or pts with medications that already inc QT interval)
Articular Cartilage Damage
DYS-GLYCEMIAS (Gatifloxacin withdrawn from market) |
|
|
Term
| Explain the major drug interactions that may occur with the fluoroquinolone antibiotics *** |
|
Definition
-Divalent and trivalent cations – ALL PO FQs
-Antacids are the most common drug interacting with FQ --the biggest problems is chelation because it impairs absorption of orally-administered FQs
-Warfarin – ALL FQs |
|
|
Term
| What are the major adverse effects associated with fluoroquinolone therapy? |
|
Definition
GI: nausea, vomiting, diarrhea, dyspepsia, C. diff colitis
CNS: headache, dizziness, insomnia, seizures(elderly)
Hepatotoxicity: not too much of a problem now but increase in proteins
Phototoxicity
Cardiac: prolongation of QT interval (worry about pts with an already prolonged QT interval or pts with medications that already inc QT interval)
Articular Cartilage Damage
DYS-GLYCEMIAS (Gatifloxacin withdrawn from market) |
|
|
Term
| Explain the major drug interactions that may occur with the fluoroquinolone antibiotics *** |
|
Definition
-Divalent and trivalent cations – ALL PO FQs
-Antacids are the most common drug interacting with FQ --the biggest problems is chelation because it impairs absorption of orally-administered FQs
-Warfarin – ALL FQs |
|
|
Term
| How does Metronidazole work? |
|
Definition
| it is a prodrug that gets activated by anaerobic reductive processes to inhibit DNA synthesis |
|
|
Term
| What is the SOA of Metronidazole? |
|
Definition
| pos and neg anaerobes such as Bacteroides, Clostridium and H. Pylori; protozoa |
|
|
Term
| What is Metronidazole used to treat clinically? |
|
Definition
| abdominal infections, diabetic foot, decubitus ulcer |
|
|
Term
| What medication does Metronidazole increase the toxicity of? |
|
Definition
|
|
Term
| What is a major side effect of Metronidazole? |
|
Definition
| seizures, peripheral neuropathy |
|
|
Term
| What ribosomal inhibitors act on the 30S subunit? |
|
Definition
Amingoglycosides
Tetracyclines |
|
|
Term
| What ribosomal inhibitors act on the 50S subunit? |
|
Definition
Chloramphenicol
Clindamycin
Macrolides
Linezolid |
|
|
Term
| What drugs have concentration-dependent killing? |
|
Definition
Azythromycin
Daptomycin
Aminoglycosides
FQs
Metronidazole
Sulfonamides (but not Bactrim) |
|
|
Term
| What drug do we want to "get in, get out" with? |
|
Definition
| Aminoglycosides -- need high peak:MIC ratio |
|
|
Term
| What antibiotic is O2 dependent? |
|
Definition
|
|
Term
| What are Aminoglycosides normally given with? |
|
Definition
| B-lactam -- to help penetrate thick PG wall |
|
|
Term
| Which Aminoglycoside treats P. aeruginosa? |
|
Definition
|
|
Term
| Which Aminoglycoside is used for highly resistant bugs? |
|
Definition
|
|
Term
| What 2 antibiotics can cause ototoxicity? |
|
Definition
| Aminoglycosides and Vancomycin |
|
|
Term
| What drugs are bacteriostatic? |
|
Definition
| Protein synthesis inhibitors except AGs |
|
|
