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60 Cards in this Set

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Bacteriostatic drugs
"We're ECSTaTiC about bacteriostatics"- Erythromycin, Clindamycin, Sulfmethoxazole, Trimethoprim, Tetracyclines, Chloramphenicol
Bacteriocidal drugs
"Very Finely Proficient At Cell Murder." Vancomycin, Fluoroquinolones, Penicillin, Aminoglycosides, Cephalosporins, Metronidazole
Penicillin G (IV), penicillin V (oral), Prototype beta-lactamase abx. Mechanism- 1. Bind penicillin binding proteins, 2. Block transpeptidase cross-linking of cell-wall. 3. Activate autolytic enzymes. Clinical use- Bacteriocidal for GPC, GPR, GNC, and spirochetes. Not penicillinase resistant. Tox- hypersensitivity rxn, hemolytic anemia. Resistance- beta-lactamase cleavage of beta-lactam ring or altered PBP in case of MRSA.
Methicillin, nafcillin, dicloacillin
Penicillinase resistant penicillins. Mechanism- same as penicillin, narrow spectrum, resistant bc of bulkier R group. Clinical use- S. aureus except MRSA-resistant bc of altered penicillin-binding protein target site. Tox- Hypersensitivity rxns, methicillin-interstitial nephritis
Ampicillin, amoxicillin
Aminopenicillins. Mechanism- Same as penicillin, wider spectrum. Penicillinase sensitive. Combine w/ penicillinase inhibitor (clavulanate) to enhance spectrum. Amoxicillin has greater oral bioavalibility than ampicillin. Clinical use- extended spectrum penicillin, HELPS orgs- H. influenzae, E. coli, Listeria, Proteus mirabilis, Salmonella, enterococci). Tox- hypersensitivity rxns, ampicillin rash, pseudomembranous colitis.
Ticarcillin, carbenicillin, piperacillin
anti-pseudomonals. Mechanism- same as penicillin. Extended spectrum. Clinical use- pseudomonas species and GNR, susceptible to penincillinase, use w/ clavulanic acid. Tox- hypersensitivity rxns
Cefazolin, cephalexin
1st generation cephalosporins. Mechanism- beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal. Clinical use- GPC, Proteus mirabilis, E. coli, Klebsiella.
Cephalosporin toxicity
Hypersensitivity rxns. Cross-hypersensitivity w/ penicillins in 5-10% of pts. Increases nephrotoxicity of aminoglycosides. Disulfiram-like rxn w/ ethanol, esp cefamandole.
Cefoxitin, cefaclor, cefuroxime
2nd generation cephalosporins. Mechanism- beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal. Clinical use- GPC, H. influenzae, Enterobacter aerogenes, Neisseria spp. Proteus mirabilis, E. coli, Klebsiella, Serratia
Ceftriaxone, cefotaxime, ceftazidime
3rd generation cephalosporins. Mechanism- beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal. Clinical use- serious GN infxns resistant to other beta-lactams; meningitis since most penetrate BBB. Ex. ceftazadime for pseudomonas, ceftriaxon for gonorrhea
4th generation cephalosporin. Mechanism- beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal. Clinical use- increased activity against Pseudomonas and GP orgs.
Mechanism- monobactam resistant to beta-lactamases. Inhibits cell wall synthesis by binding to PBP3. Synergistic w/ aminoglycosides. No cross-allerginicity w/ penicillins. Clinical use- GNR- Klebsiella, Pseudomonas, Serratia. No activity against GP or anaerobes. For penicillin-allergic pts and those w/ renal insufficiency who cannot tolerate aminoglycosides. Tox- occasional GI upset.
Imipenem/cilastatin, meropenem
Carbapenems. Mechanism- broad-spectrum beta-lactamase-resistant. Imipenem Administered w/ cilastatin to decrease inactivation by renal tubules. Clinical use- GPC, GNR, anarobes. Drug of choice for enterobacter. Limit to life threatening infxn bc of tox. Meropenem has reduced risk of seizures. Tox- GI distress, skin rash, CNS tox- seizures at high plasma levels.
Mechanism- inhibit cell wall mucopeptde formation by binding D-ala-D-ala portion of cell wall precursors. Bactericidal. Resistance occur w/ AA change of D-ala-D-ala to D-ala-D-lac. Clinical use- Used for serious GP, MDR organisms including S. aureus and C. dificile. Tox- nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing-red man syndrome- prevent by slow infusion rate and antihistamines. Well tolerated in general
30s inhibitors
Aminoglycosides (bacteriocidal), Tetracylines (bacteriostatic)
50s inhibitors
Chloramphenicol, Clindamycin (bacteriostatic), Erythromycin (bacteriostatic), Lincomycin(bacteriostatic), Linezolid (variable)
Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin
Aminoglycosides. Mechanism- bactericidal. Inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for uptake therefore ineffective against anaerobes. Clinical use- Severe GNR infections, Synergistic w/ Beta-lactam abx. Neomycin for bowl surgery. Tox- nephrotoxicity (esp when used w/ cephalosporins), Ototoxicity (esp when used w/ loop diuretics), Teratogen. Resistance- modification via acetylation, adenylation, phosphorylation.
Tetracycline, doxycycline, demclocycline, minocycline
Tetracyclines. Mechanism- Bacteriostatic. Bind to 30s and prevent attachment of aminoacyl-tRNA, limited CNS penetration. Doxycycline is fecally eliminated and can be used in pts in renal failure. Must NOT be taken w/ milk, antacids, or iron-containing preparations inhibit absorption. Clinical use- "VACUUM THe BedRoom" - Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Tularemia, H. pylori, Borrelia burgdorferi, Rickettsia. Tox- GI distress, discoloration of teeth and bone growth inhibition in children, photosensitivity. Contrindicated in pregnancy. Resistance- decreased uptake or increased transport out of cell
Erythromycin, Azithromycin, Clarithromycin
Macrolides- Mechanism- Inhibit protein synthesis by blocking translocation. Bind to 23s rRNA of 50s ribosomal subunit. Bacteriostatic. Clinical use- URIs, pneumonia, STDs, GPC (good for strep infxns in pts allergic to penicillin), Mycoplasma, Legionella, Chlamydia, Neisseria. Tox- prolonged QT, GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophylline and oral anticoagulants. Resistance- methylation of rRNA near erythromycin ribosome-binding site
Mechanism- Inhibits 50s peptidyltransferase activity. Bacteriostatic. Clinical use- Meningitis (SHiN), conservative use due to tox. Tox- dose dependent anemia, aplastic anemia (dose independent), gray baby syndrome in premature infants bc they lack UDP-glucuronyl transferase. Resistance- modification via acetylation.
Mechanism- blocks peptide bond formation at 50S ribosomal subunit. Bacteriostatic. Clinical use- anaerobic infxns (Bacteroides fragilis, C. perfringens). Tox- C. dificile overgrowth, fever, diarrhea.
Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine
Mechanism- PABA antimetabolites inhibit dihydropteroate synthetase. Bacteriostatic. Clinical use- GP, GN, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI. Tox- Hypersensitivity rxn, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin like warfarin. Resistance= altered enzyme, decreased uptake, increased PABA synthesis
Mechanism- Inhibits bacterial dihydrofolate reductase. Bacteriostatic. Clinical use- in combo w/ SMX causing sequentioal block of folate synthesis. Combination used for recurrent UTI, Shigella, Salmonella, Pneumocystis jiroveci. Tox- megaloblastic anemia, leukopenia, granulocytopenia
Ciprofloxacin, norfloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, enoxacin. Nalidixic acid.
Fluoroquinolones. Nalidixic acid=quinolone. Mechanism- Inhibit DNA gyrase (topoisomerase II). Bactericidal. Must not be be taken w/ antacids. Clinical use- GNR of urinary and GI tracts including Pseudomonas, Neisseria, some GP org. Tox- GI upset, superinfections, skin rashes, headache, dizziness. Contraindicated in pregnant women and children bc of damage to cartilage. Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids. Resistance- altered gyrase or reduced uptake
Mechanism- forms toxic metabolites in the bacterial cell that damage DNA. Batericidal, antiprotozoal. Clinical use- Giardia, Entamoeba, Trichomonas, Gardenerella vaginalis, Anaerobes (Bacteroides, Clostridium). Used w bismuth and amoxicillin or tetracycline for H. pylore triple therapy. Tox- Disulfiram-like rxn w/ alcohol, headaches, metallic taste
Polymyxin B and E. Mechanism- Bind to cell membranes of bacteria and disrupt their osmotic properties. Polymyxins are cationic, basic protein that act like detergents. Clinical use- resistant GN infections. Tox- Neurotoxicity, acute renal tubular necrosis.
M. tuberculosis treatment
Prophylaxis- Isoniazid. Tx-Isoniazid, Rifampin, Ethambutol, Pyrazinamide. Also streptomycin, cycloserine (2nd line). Ethambutol tox- optic neuropathy. Tox others- hepatotox
M. avium-intracellulare
Prophylaxis- Azithromycin, Tx- azithromycin, rifampin, ethambutol, streptomycin.
M. leprae
Prophylaxis- none. Tx-dapsone, rifampin, clofazimine
Mechanism- decreased synthesis of mycolic acids. Clinical use- TB prophylaxis and tx in combo. Tox- neurotox, hepatotox. Vitamin B6/Pyridoxine can prevent neurotox
Mechanism- Inhibits DNA-dependent RNA pol. Clinical use- TB. Delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children w/ H. influenzae type B. Tox- minor hepatotox, increase P-450 activity, orange body fluids. Rimfampin 4Rs- RNA pol inhibitor, Revs up microsomal P450, Red/oRange body fluids, Rapid resistance if used alone
meningococcal prophylaxis
rimfampin, minocycline
Benzathine penicillin G
Hx of recurrent UTI
Pneuomocystis jiroveci pneumonia
TMP-SMX, aerosolized pentamidine
Endocarditis with surgical or dental procedures
VRE tx
linezolid and streptogramins (quinupristin/dalfopristin)
Amphotericin B
Mechanism- binds ergosterol, forms membrane pores that allow leakage of electrolytes. Clinical use- used for wide spectrum of systemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor. Intrathecally for fungal meningitisl does not cross BBB. Tox- fever/chills, hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis. Hydration reduces nephrotoxicity. Liposomal amphotericin reduces toxicity.
Mechanism- binds ergosterol, disrupting fungal membranes, too toxic for systemic use. Clinical use- swish and swallow for thrush, topical for diaper rash or vaginal candidiasis
fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole
Azoles. Mechanism- inhibit fungal serol synthesis. Clinical use- systemic mycoses. Flu- for cryptococcal meningitis in AIDS pts (it can cross BBB) and candidal infxns of all types. Ket- for blastomyces, Coccidioides, Histoplasma, Candida albicans, hypercortisolism. Clotrim- and micon- for topical fungal infxns. Tox- hormone synthesis inhibition (gynecomastia), liver dysfxn due to inhibition of P450, fever, chills
Mechanism- inhibit DNA synthesis by conversion to 5-fu. Clinical use- systemic fungal infxns (Cryptococcus, Candida) in combination w/ amphotericin B. Tox- nausea, vomiting, diarrhea, bone marrow suppression
Mechanism- inhibit cell wall synthesis by inhibiting synthesis of beta-glucan. Clinical use- invasive aspergillosis. Tox- GI upset, flushing
Mechanism- inhibits fungal enzyme squalene epoxidase. Clinical use- tx dermatophytes esp onchomycosis
Mechanism- interferes with microtubule fxn, disrupts mitosis. Deposits in keratin-containing tissues like nails. Clinal use- oral tx of superficial infxns, inhibits growth of dermatophytes (tinea, ringworm). Tox- teratogenic, carcinogenic, confusion, headaches, increase P-450 and warfarin metabolism
Mechanism- blocks viral penetration/uncoating (M2 protein); may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. Clinical use- prophylaxis and tx for influenza A and rubella, Parkinson's dz. Tox- ataxia, dizziness, slurred speech. Resistance- Mutated M2 protein. 90% of all flu A strains are resistant to amantadine so not used. Rimantidine is a derivative w/fewer CNS side effects.
Zanamivir, oseltamivir
Mechanism- inhibit influenza neuroaminidase, decreasing release of progeny virus. Clinical use- influenza A and B
Mechanism- inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase. Clinical use- RSV, chronic hepatitis C. Tox- hemolytic anemia. Severe teratogen.
Mechanism- monophosphrylated by HSV/VZV thymidine kinase. Guanisine analog. Triphosphate formed by cellular enzymes. Preferentially ihibits viral DNA pol by chain termination. Clinical use- HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocomp pts. For herpes zoster use famciclovir (related drug). No effect on latent forms of VZV and HSV. Tox- generally well tolerated. Resistance- lack of thymidine kinase
Mechanism- 5'monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA pol. Clinical use- CMV, esp immunocomp pts. Tox-leukopenia, neutropenia, thrombocytopenia, renal tox. More toxic to host enzymes than acyclovir. Resistance- mutated CMV DNA pol or lack of viral kinase
Mechanism- Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase. Clinical use- CMV retinitis when ganciclovir fails. Acyclovir-resistant HSV. Tox-nephrotoxicity. Resistance- mutated DNA pol
Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir
HIV Protease inhibitors. Mechanism- inhibit maturation of new virus by blocking protease in progeny virions. Tox- GI intolerance (nause, diarrhea), hyperglycemia, lipodystrophy, thrombocytopenia (indinavir)
Zidovudine (ZDV formerly AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), abacavir
Nucleoside reverse transcriptase inhibitors
Nevirapine, Efavirenz, Delavirdine
Non-nucleoside reverse transcriptase inhibitors.
Reverse transcriptase inhibitors
Mechanism- preferentially inhibit reverse transcriptase of HIV; prevent incorporation of DNA copy of viral genome into host DNA. Tox- bone marrow suppression (neutropenia, anemia use GM-CSF and Epo to counteract), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV). Clinical use- HAART
Highly active antiretroviral therapy. Combination therapy w/ protease inhibitors and reverse transcriptase inhibitors. Initiated when CD4²500 or high viral load. ZDV is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission
HIV fusion inhibitor. Mechanism- bind gp41 subunit, inhibit conformational change required for fusion w/ CD4 cells and therefore block entry and subsequent replication. Tox-hypersensitivity rxn, rxn at subq injxn site, increased risk of bacterial pneumonia. Clinical use- in pts. w/ persistent viral replication in spite of antiretroviral therapy. Used in combination w/ other HIV drugs.
Mechanism- Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis. Induce ribonuclease that degrades viral mRNA. Clinical use- IFN-alpha-chronic hep B and C, Kaposi's sarcoma. IFN-beta- MS. IFN-gamma- NADPH oxidase deficiency. Tox- Neutropenia
Abx to avoid in pregnancy
SAFE Moms Take Really Good Care- Sulfonamides-kernicterus; Aminoglycoside- ototoxicity; Fluoroquinolones- cartilage damage; Erythromycin- acute cholestatic hepatis in mom, clarithromycin is embrotoxic; Metronidazoles- mutagenesis; Tetracycines- discolored teeth, inhibition of bone growth; Ribavirin- teratogenic; Griseofulvin- teratogenic; Chloramphenicol- gray baby