Glossary of First Aid: Antimicrobials
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- Block cell wall synthesis by inhibiting peptidoglycan cross-linking.
- penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam, cephalosporins
- Block peptidoglycan synthesis.
- bacitracin, vancomycin, cycloserine
- Block protein synthesis at 50S ribosomal subunit.
- chloramphenicol, erythromycin/macrolides, lincomycin, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid
- Block protein synthesis at 30S ribosomal subunit.
- aminoglycosides, tetracyclines
- Block DNA topoisomerases.
- Block mRNA synthesis
- Bactericidal antibiotics.
- penicillin, cephalosporins, vancomycin, aminoglycosides, fluoroquinolones, metronidazole
- Disrupt bacterial/fungal cell membranes
- Disrupt fungal cell membranes.
- amphotericin B, nystatin, fluconazole/azoles
- Penicillin (G: IV form; V: oral form)
- M: binds PBPs, blocks transpeptidase cross-linking of cell wall, activates autolytic enzymes; 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; 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; C: extended spectrum penicillin, certain gram + bacteria and gram - rods (ampicillin/amoxicillin HELPS kill enterococci - Haemophilus influenza, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enterococci); T:hypersensitivity reactions, ampicillin rash, pseudomembranous colitis.
- 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
- 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)
- M: monobactam resistant to beta lactamases, inhibits cell wall synthesis (binds to PBP3), synergistic with aminoglycosides, no cross-allergenicity with penicillins; 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.
- 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; 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."
- 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; 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
- M: inhibits 50S peptidyltransferase, bacteriostatic; 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)
- M: blocks peptide bond formation at 50S ribosomal subunit, bacteriostatic; C: treat anaerobic infections (eg.: Bacteroides fragilis, Clostridium perfringens); T: pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea
- eg.: sulfamethoxazole (SMX), sulfisoxazole, triple sulfas, sulfadiazine
M: PABA antimetabolites inhibit dihydropteroate synthase; bacteriostatic
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 = TMP = "Treat Marrow Poorly"
C: combined with sulfas to cause sequential block of folate synthesis; combo used for recurrent UTIs, Shigella, Salmonella, Pneumocystis carinii pneumonia
T: megaloblasticanemia, leukopenia, granulocytopenia (can alleviate with supplemental folinic acid)
- "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
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
- 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
- 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
C: resistant gram - infections
T: neurotoxicity, acute renal tubular necrosis
- anti-TB drugs
- RESPIre. All are hepatotoxic.
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
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's 4 R's:
RNA polymerase inhibitor
Revs up microsomal P-450
Red/orange body fluids
Rapid resistance if used alone
- block nucleotide synthesis
- sulfonamides, trimethoprim
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