Antimicrobials Flashcards
Learn the major classes of antimicrobials, the drugs in each, what class a drug belongs to, and the mechanism of action of each class. Specific resistance mechanisms and pharmacokinetics/ROA indications are not covered. MOA = mechanism of action
4 ways bacteria resist antimicrobials
Alter receptor target; decrease entry in or out of; alter metabolic pathway; inactivate drug directly
Mechanisms of antimicrobial action
Inhibit: cell wall synthesis, protein synthesis, folic acid synthesis, or DNA/RNA synthesis
Penicillins mechanism of action
Inhibit cell wall synthesis by binding to transpeptidase, a PBP, preventing cell wall peptidoglycan layer synthesis
Natural penicillins
Penicillin G and V
Penicillin G ROE
IM or IV
Natural penicillins microbe targets
G+
Penicillin V ROE
oral on empty stomach
Ampopenicillins
Ampicillin and amoxicillin
Ampopenicillins ROE
Enteral or parenteral
Penicillinase-resistant penicillins
dicloxacillin, methicillin, oxacillin, nafcillin
Penicillinase-resistant penicillins are named because
Side groups prevent B-lactmases from degrading them
Irreversible B-lactamase inhibitors
Clavulanic acid, sulbactam, tazobactam
People allergic to penicillins shouldn’t take this class of antibiotics
Cephalosporins
B-lactams MOA
cell wall synthesis
Vancomycin MOA
cell wall synthesis
Trimethoprim MOA
Folic acid synthesis (dihydrofolate reductase inhibition)
Sulfonamides MOA
Inhibits folic acid production (dihydropteroate synthetase inhibition - upstream from Trimethoprim)
Quinolones MOA
DNA synthesis
Rifampin MOA
Inhibits bacterial RNA polymerase; used for mycobacterial infections
Chloramphenicol MOA
Protein synthesis - 50S
Macrolides MOA
Protein synthesis - 50S
Clindamycin MOA
Protein synthesis - 50S
Tetracyclines MOA
Protein synthesis - 30S
Aminoglycosides MOA
Protein synthesis - 30S
Monobactams MOA
Cell wall synthesis
Carbapenems MOA
Cell wall synthesis
These penicillin classes are used to treat G+
Natural penicillins and penicillinase-resistant penicillins
These penicillin classes are used to treat G-
Aminopenicillins and antipseudomonal penicillins
Antipseudomonal penicillins
Carbenicillin, ticarcillin, mezlocillin, piperacillin
This drug when administered orally is limited in use to treating UTIs
carbenicillin
B-lactamase inhibitors
Clavulanic acid, sulbactam, tazobactam
Combine this class of drug with penicillins to broaden spectrum
Irreversible B-lactamase inhibitors
Carbapenems
imipenem/cilastatin, doripenem, ertapenem, meropenem
Carbapenems - bactericidal or bacteriostatic?
Bactericidal
Carbapenems have this advantage over penicillins and cephalosporins
B-lactamase resistant
Other cell wall disrupters
telavancin, vancomycin
Vancomycin MOA
Blocks polymerization and cross-linking of peptidoglycan by binding to Ala-Ala pair
Cycloserine MOA
Blocks cell wall synthesis in G+ and G-
Cycloserine is usually reserved for this disease
TB
Polymyxin B MOA
Disrupts PM in all G- except Proteus
Aminoglycosides
Amikacin, gentamicin, kanamycin, netilmicin, streptomycin, tobramycin, neomycin
Aminoglycosides are limited to treating this type of bacterial infection
G-
Major side effects of aminoglycosides
Ototoxicity and nephrotoxicity via accumulation due to high water solubility
Antimicrobial effect observed even as aminoglycoside [plasma] decreases
Postantibiotic effect - translation still inhibited
Tetracyclines
tetracycline, minocycline, doxycycline, demeclocycline, oxytetracycline, tigecycline
Absorption of tetracyclines may be inhibited by these
Divalent cations (Ca2+, Mg2+) = don’t take with milk or antacids!
This tetracycline is safest for patients with renal dysfunction and say why
Doxycycline because it is excreted in feces
Lincosamides
clindamycin
Clindamycin MOA
Binds 50S subunit and prevent translation
Macrolides
erythromycin + anything = macrolide; clarithromycin, azithromycin
Erythromycins have this significant cardiovascular side effect - except one member of the class
Prolong TQ interval which can lead to fatal arrythmia - azithromycin doesn’t do this
Ketolides
Telithromycin
Ketolides MOA
Bind 50S in two different domains, requiring 2 mutations to develop resistance
Retapamulin MOA
A “pleuromutlin” antibiotic that blocks protein synthesis by interfering with peptidyl transferase, preventing 50S formation
Penicillin G
Natural penicillin (readily destroyed in acidic environments so only IV or IM)
Penicillin V
Natural penicillin (oral administration on empty stomach)
Ampicillin
Aminopenicillin (enteral or parenteral)
Amoxicillin
Aminopenicillin (enteral or parenteral)
Dicloxacillin
Penicillinase-resistant penicillins
Dicloxacillin
Penicillinase-resistant penicillins
Methicillin
Penicillinase-resistant penicillins
Oxacillin
Penicillinase-resistant penicillins
Nafcillin
Penicillinase-resistant penicillins
Carbenicillin
Antipseudomonal penicillin
Ticarcillin
Antipseudomonal penicillin
Mezlocillin
Antipseudomonal penicillin
Piperacillin
Antipseudomonal penicillin
Clavulanic acid
B-lactamase inhibitor
Sulbactam
B-lactamase inhibitor
Tazobactam
B-lactamase inhibitor
Iminipenem/clastatin
Carbapenems
Doripenem
Carbapenems
Ertapenem
Carbapenems
Meropenem
Carbapenems
Telavancin
Other cell wall inhibitors
Vancomycin
Other cell wall inhibitors
Cycloserine
Other cell wall inhibitors
Polymyxin B
Other cell wall inhibitors
Amikacin
Aminoglycosides (protein synthesis inhibitors)
Gentamicin
Aminoglycosides
Kanamycin
Aminoglycosides
Netilmicin
Aminoglycosides
Streptomycin
Aminoglycosides
Tobramycin
Aminoglycosides
Neomycin
Aminoglycosides
Tetracyclines are easy to name because
they all have -cycline
Clindamycin
Lincosamide
Erythromycin and its derivatives
Macrolides
Clarithromycin
Macrolides
Azithromycin
Macrolides
Telithromycin
Ketolides
Streptogramins are a combination of these
Quinupristin and dalfopristin
Sulfa-anything
Sulfonamides
Any-floxacin
Fluoroquinolones
Fluoroquinolones MOA
Inhibit DNA synthesis (DNA gyrase or topoisomerase IV)
Daptomycin
Lipopeptides
Linezolid MOA
Binds 50S subunit preventing 70S formation
Mupirocin has a unique MOA and usability because…
No cross-resistance risk; inhibits tRNA that transports isoleucine
Metronidazole MOA
Absorbed only be anaerobes and some protozoans; its metabolism generates toxic metabolites that inhibit DNA synthesis (mutagenic and possibly carcinogenic so contraindicated during 1st trimester)
Nitazoxanide MOA
Interferes with pyruvate electron transfer, necessary for anaerobic matabolism
Tinidazole MOA
Damages DNA and inhibits further synthesis (thus is mutagenic and possibly carcinogenic and contraindicated during 1st trimester)
Daptomycin MOA
Binds to bacterial PM and disrupts membrane potential, causing rapid depolarization and inhibition of DNA/RNA/protein synthesis (so unique that no cross-resistance known)
Rifaximin MOA
Binds bacterial RNA polymerase
Isoniazid MOA
Inhibits mycolic acid synthesis, which is required by mycobacteria
Pyrazinamide MOA
Unclear (but we have to know it?) but may lower pH in tubercle cavity
Ethambutol MOA
Inhibits RNA synthesis (mycobacteria)
Clofazimine MOA
Inhibits mycobacterial RNA polymerase