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60 Cards in this Set

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What drugs Block cell wall synthesis by inhibiting peptidoglycan cross-linking.
penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam, cephalosporins
What drugs Block peptidoglycan synthesis.
bacitracin, vancomycin, cycloserine
What drugs Block protein synthesis at 50S ribosomal subunit.
chloramphenicol, erythromycin/macrolides, lincomycin, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid
What drugs Block protein synthesis at 30S ribosomal subunit.
aminoglycosides, tetracyclines
What drugs Block DNA topoisomerases.
quinolones
What drugs Block mRNA synthesis
rifampin
What drugs Bactericidal antibiotics.
penicillin, cephalosporins, vancomycin, aminoglycosides, fluoroquinolones, metronidazole
What drugs Disrupt bacterial/fungal cell membranes
polymyxins
What drugs Disrupt fungal cell membranes.
amphotericin B, nystatin, fluconazole/azoles
What is the mechanism of pentamide?
its mechanism is unknown
Penicillin (G: IV form; V: oral form)
M: binds PBPs, blocks transpeptidase cross-linking of cell wall, activates autolytic enzymes;
Penicillin (G: IV form; V: oral form): clinical use and toxicity
C: bactericidal for gram + cocci, gram + rods, gram - cocci and spirochetes; T: hypersensitivity reactions, hemolytic anemia.
Methicillin, nafcillin, dicloxacillin
M: binds PBPs, blocks transpeptidase cross-linking of cell wall, activates autolytic enymes; narrow spectrum; penicillinase resistant because of bulkier R group;
Methicillin, nafcillin, dicloxacillin: clinical use and toxicity
C: staphylococcus aureus; T: hypersensitivity reactions; methcillin - interstitial nephritis.
Ampicillin, amoxicillin
M: binds PBPs, blocks transpeptidase cross-linking of cell wall, activates autolytic enymes; wider spectrum, penicillinase sensitive, can combine with clavulanic acid (penicillinase inhibitor) to enhance spectrum; amOxicillin = Oral bioavailability;
Carbenicillin, piperacillin, ticarcillin
M: binds PBPs, blocks transpeptidase cross-linking of cell wall, activates autolytic enymes; extended spectrum;
C: pseudomonas spp. and gram - rods; susceptible to penicillinase; use with clavulanic acid; T: hypersensitivity.
Cephalosporin mechanism
beta lactam drugs that inhibit cell wall synthesis, but less vulnerable to penicillinases; bactericidal
1st generation cephalosporins: clinical use
PEcK: gram + cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae

mainly for surgery prophylaxis
2nd generation cephalosporins: clinical use
HEN PEcKS: gram + cocci, Haemophilus influenza, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens
3rd generation cephalosporins: clinical use
serious gram - infections resistant to other beta lactams, meningitis (most penetrate the BBB); eg.: ceftazidime for pseudomonas, ceftriaxone for gonorrhea
4th generation cephalosporins: clinical use
increased activity against pseudomonas and gram + organisms
Cephalosporin toxicity
hypersensitivity reactions, + nephrotoxicity of aminoglycosides, disulfiram-like reaction with ethanol (in cephalosporins with a methylthiotetrazole group, eg.: cefmandole)
Aztreonam
M: monobactam resistant to beta lactamases, inhibits cell wall synthesis (binds to PBP3), synergistic with aminoglycosides, no cross-allergenicity with penicillins;
aztreonam: clinical use and toxicity
C: gram - rods (Klebsiella spp., Pseudomonas spp., Serratia spp.), no activity agains gram + or anaerobes, for use in penicillin-allergic patients and those with renal insufficiency who can't tolerate aminoglycosides; T: usually non-toxic; occasional GI upset.
Imipenem/cilastatin
M: imipenem is a broad-spectrum, beta lactamase resistant carbapenem, always administered with cilastatin (inhibitor of renal dihydropeptidase I) to lower inactivation in renal tubules;
imipenem/ cilastatin: clinical use and toxicity
C: gram + cocci, gram - rods, and anaerobes (drug of choice for Enterobacter); T: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels
Imipenem/cilastatin mneumonic
with imipenem, "the kill is LASTIN' with ciLASTATIN."
Vancomycin
M: block cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors, bactericidal, resistance occurs with amino acid change of D-ala D-ala to D-ala D-lac;
vancomycin: clinical use and toxicity
C: used for serious gram + multi-drug resistant organisms, including Staph aureus and Clostridium difficile (pseudomembranous colitis); T: "well tolerated in general, does NOT have many problems." Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing ("red man syndrome" - can be largely prevented by pretreatment with antihistamines and slow infusion rate
List the protein synthesis inhibitors
"buy AT 30, CELL at 50": 30S inhibitors...Aminoglycosides ("TAGS" tobramycin, amikacin, gentamicin, streptomycin [bactericidal]), Tetracylines [bacteriostatic]; 50S inhibitors...Chloramphenicol, Erythromycin, Lincomycin, cLindamycin [all 4 are bacteriostatic]
List the aminoglycosides and their mechanism of action
TANGS: tobramycin, amikacin, neomycin, gentamicin, streptomycin; M: bactericidal, inhibit formation of initiation complex and cause misreading of mRNA, require O2 for uptake so ineffective against aerobes.
Aminoglycosides: clinical use and toxicity
C: severe gram - rod infections, synergistic with beta lactam antibiotics, neomycin for bowel surgery; T: Nephrotoxicity (esp. when combined with cephalosporins), Ototoxicity (esp. when combined with loop diuretics) "amiNOglycosides"
List the tetracyclines and their mechanism of action
TDDM: tetracyline, doxycycline, demeclocycline, minocycline; bacteriostatic, bind to 30S and prevent attachment of aminoacyl tRNA, limited CNS penetration; doxycycline is fecally eliminated and can be used in patients with renal failure; must NOT be taken with milk, antacids, or iron-containing prepartions because divalent ions inhibit gut absorption
Tetracylines: clinical use and toxicity
C: VACUUM you BedRoom: Vibrio cholerae, Acne, Chlamydia, Ureaplasma Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi (Lyme disease), Rickettsia, tularemia; T: GI distress, discoloration of teeth and inhibition of bone growth in children, Fanconi's syndrome, photosensitivity.
List the macrolides and their mechanism of action
ACE: azithromycin, clarithromycin, erythromycin; M: inhibit protein synthesis by blocking translation, bind to the 23S rRNA of the 50S ribosomal subunit, bacteriostatic
Macrolides: clinical use and toxicity
C: URIs, pneumonias, STDs (gram + cocci; streptococcal infections in patients allergic to penicillin), Mycoplasma, Legionella, Chlamidia, Neisseria; T: GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis, eosinophilia, skin rashes
Chloramphenicol
M: inhibits 50S peptidyltransferase, bacteriostatic;
chloramphenicol: clinical use and toxicity
C: meningits (H. influenza, N. meningitidis, S. pneumoniae); T: use conservatively due to the toxicities - anemia (dose dependent), aplastic anemia (dose dependent), gray baby syndrome (in premature infants because they lack liver UDP-glucoronyl transferase)
Clindamycin
M: blocks peptide bond formation at 50S ribosomal subunit, bacteriostatic;
Clindamycin: clinical use and toxicity
C: treat anaerobic infections (eg.: Bacteroides fragilis, Clostridium perfringens); T: pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea
sulfonamides
eg.: sulfamethoxazole (SMX), sulfisoxazole, triple sulfas, sulfadiazine M: PABA antimetabolites inhibit dihydropteroate synthase; bacteriostatic
sulfonamides: clinical use
C: gram +, gram -, nocardia, chlamydia; triple sulfas or SMX for simple UTI T: hypersensitivity rxn, hemolysis if G6PD deficient nephrotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (eg. warfarin)
sulfonamides: toxicity
C: gram +, gram -, nocardia, chlamydia; triple sulfas or SMX for simple UTI T: hypersensitivity rxn, hemolysis if G6PD deficient nephrotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (eg. warfarin)
why is THF (tetrahydrofolic acid) important?
cofactor in the production of purines and the amino acids thymine, methionine and glycine
trimethoprim
trimethoprim = TMP = "Treat Marrow Poorly"
trimethoprim: clinical use
C: combined with sulfas to cause sequential block of folate synthesis; combo used for recurrent UTIs, Shigella, Salmonella, Pneumocystis carinii pneumonia
trimethoprim: toxicity
T: megaloblasticanemia, leukopenia, granulocytopenia (can alleviate with supplemental folinic acid)
fluoroquinolones
"FluoroquinoLONES hurt attachments to your BONES" eg.: ciprofloxacin, norfloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, enoxacin (fluoroquinolones), nalidixic acid (a quinolone) M: inhibit DNA gyrase (topoisomerase II), bactericidal
fluoroquinolones: clinical use and toxicity
C: gram - rods of urinary and GI tracts (incl. Pseudomonas), Neisseria, some gram + organisms T: GI upset, superinfection, skin rashes, headache, dizziness; contraindicated in pregnant women and kids due to possible cartilage damage; tendonitis and tendon rupture in adults
metronidazole
GET on the METRO! Anaerobes below the diaphragm M: forms toxic metabolites in the bacterial cell; bactericidal C: antiprotozoal, Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (Bacteroides, Clostridium); used with bismuth and amoxicillin (or tetracyline) for "triple therapy" against H. pylori T: disulfram-like reaction with alcohol, headache
metronidazole:clinical use and toxicity
C: antiprotozoal, Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (Bacteroides, Clostridium); used with bismuth and amoxicillin (or tetracyline) for "triple therapy" against H. pylori T: disulfram-like reaction with alcohol, headache
polymyxins
eg.: polymyxin B, polymyxin E M: bind to cell membranes of bacteria and distrupt osmotic properties; polymyxins are cationic, basic proteins that act like detergents
polymyxins: clinical use and toxicity
C: resistant gram - infections T: neurotoxicity, acute renal tubular necrosis
anti-TB drugs
RESPIre. All are hepatotoxic. Rifampin Ethanmbutol Steptomycin Pyrazinamide Isoniazid (INH) cycloserine (2nd line therapy)
isoniazid (INH)
INH Injures Neurons and Hepatocytes. Different INH half lives in fast vs. slow acetylators. M: - synthesis of mycolic acids
isoniazid (INH): clinical use and toxicity
C: Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB. T: Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicity, SLE-like syndrome. Pyridoxine (vitamin B6) can prevent neurotoxicity.
rifampin
Rifampin's 4 R's: RNA polymerase inhibitor Revs up microsomal P-450 Red/orange body fluids Rapid resistance if used alone
Rifampin: mechasnism of action
inhibits DNA dependent RNA polymerase
rifampin: clinical use and toxicity
M. tuberculosis; delays resistance to dapsone when used for leprosy; used for meningococcal prophylaxis and chemoprophylaxis in contacts with childresn with Haemophilus Influenza type B. T: minor hepatotoxicity and Drug interactions (increases p450)