Ch. 9 - Chemotherapy

Cards (26)

  • selective toxicity
    ability of drug to kill or inhibit pathogen while damaging host as little as possible
  • therapeutic dose
    drug level required for clinical treatment
  • toxic dose
    drug level at which drug becomes too toxic for patient, produces side effects
  • therapeutic index
    ration of toxic does to therapeutic dose
  • narrow-spectrum drugs
    attack only a few different pathogens
  • broad-spectrum drugs
    attack many different pathogens
  • minimal inhibitory concentration
    lowest concentration of drug that inhibits growth of pathogen
  • minimal lethal concentration
    lowest concentration of drug that kills pathogen
  • dilution susceptibility tests
    inoculating media containing different concentrations of drug to test for MIC and MLC
  • e test
    similar to disc diffusion but with strips that contain a gradient of an antibiotic, for use with anaerobic pathogens
  • penicillins
    inhibit cell wall synthesis by blocking the enzyme that catalyzes the links in peptidoglycan leading to lysis of cell; acts only on growing bacteria, can also bind to PBPs, activate autolysins, or stimulate holins to form holes in the membrane
  • cephalosporins
    broad-spectrum drugs that can be used when a patient is allergic to penicillin
  • vancomycin and teicoplanin
    glycopeptide drugs that inhibit cell wall synthesis, important for treatment in MRSA/E infections
  • aminoglycosides
    inhibit protein synthesis by binding to 30S ribosomal subunit and cause the misreading of the mRNA
  • tetracyclines
    broad-spectrum and bacteriostatic drugs that inhibit protein synthesis by binding to the 30S ribosomal subunit and stops bind of aminoacul-tRNA molecules to the A site of the ribosome
  • macrolides (erythromycin, clindamycin, zithromax)

    broad-spectrum bacteriostatic drugs that inhibit protein synthesis by binding to the 23S and 50S ribosomal subunits to stop peptide chain elongation; used for patients allergic to penicillin
  • chloramphenicol
    inhibits protein synthesis by binding to the 23S and 50S ribosomal subunits and stopping peptidyl transferase reactions; toxic, not used often
  • sulfonamides
    antimetabolites that are structurally similar to PABA, which is used for the synthesis of folic acid which is a precursor to nucleic acids
  • trimethoprim
    broad-spectrum antimetabolite that blocks DHFR in folic acid pathway; has lots of side effects
  • quinolones
    broad-spectrum drugs that inhibit NA synthesis by stopping bacterial DNA-gyrase and topoisomerase II
  • mycoses
    topical and oral treatments like candida that disrupt membrane permeability and inhibit sterol synthesis; may inhibit protein and DNA synthesis by disrupting mitotic spindle
  • systemic mycoses
    difficult to treat and often fatal, amp B binds to sterols in membranes, 5-flucytosine disrupts RNA function, and fluconazol (preventative)
  • antiprotozoans
    antiviral drugs that block steps in NA synthesis, ETC, protein synthesis and folic acid production
  • mechanisms of drug resistance
    prevent entrance of drug, drug efflux, chemical inactivation of drug, modification of target enzyme or organelle, and use of alternative metabolic pathways
  • immunity genes
    resistance genes that exist in nature to protect antibiotic producing microbes from their own antibiotics
  • horizontal gene transfer

    transferred immunity genes from antibiotic producers to non-producers