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148 Cards in this Set
- Front
- Back
Nystatin
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Antifungal
MOA: Bind to ergosterol in plasma membrane to form pores; K+ leakage *More toxic than amphotericin B |
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Amphotericin B
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Antifungal
MOA: Bind to ergosterol in plasma membrane to form pores; K+ leakage SE: Renal toxicity, fever and chills |
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Miconazole
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Antifungal - Azole
Topical PK: Inhibits P450 (3A4) MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability SE: Hepatitis |
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Ketoconazole
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Antifungal - Azole
Oral PK: Inhibits P450 (3A4) SE: **Blocks androgen and adrenal steroid synthesis (gynecomastia), fatal hepatotoxic, hepatitis MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability Important! |
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Clotrimazole
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Antifungal - Azole
Topical PK: Inhibits P450 (3A4) MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability SE: Hepatitis |
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Fluconazole
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Antifungal - Azole
*Does not inhibit steroidogenesis, no endocrine SE DOC for cryptococcus neoformans, candidemia MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability SE: Hepatitis |
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Itraconazole
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Antifungal - Azole
PK: Inhibits P450 (3A4) MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability SE: Hepatitis |
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Caspofungin
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Antifungal
MOA: Inhibit synthesis of fungal cell wall, inhibit synthesis of B-1,3-D- glucan Important! |
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Flucytosine
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Antifungal
MOA: Cytosine deaminase converts flucytosine to 5-flurodeoxyuridine (5-FU, a false analog) inhibiting thymidylate synthase. |
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Griseofulvin
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Antifungal
MOA: Binds to microtubules to inhibit mitosis PK: Induces P450 SE: Hepatitis |
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Mechlorethamine
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Alkylating Agent
Electrophiles that react with electron-rich atoms (DNA) in the cells to form covalent cross links which causes inhibition of DNA replication. SE: Myelosuppression and secondary leukemia |
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Cyclophosphamide
|
Alkylating Agent
Electrophiles that react with electron-rich atoms (DNA) in the cells to form covalent cross links which causes inhibition of DNA replication. SE: Myelosuppression and secondary leukemia *Mesna co-administered to prevent hemorrhagic cystitis Important! |
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Melphalan
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Alkylating Agent
Electrophiles that react with electron-rich atoms (DNA) in the cells to form covalent cross links which causes inhibition of DNA replication. SE: Myelosuppression and secondary leukemia |
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bis-chloroethyl nitrosourea (BCNU)
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Alkylating Agent
Electrophiles that react with electron-rich atoms (DNA) in the cells to form covalent cross links which causes inhibition of DNA replication. SE: Myelosuppression and secondary leukemia *Additional SE: CNS abnormalities |
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Busulfan
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Alkylating Agent
Electrophiles that react with electron-rich atoms (DNA) in the cells to form covalent cross links which causes inhibition of DNA replication. SE: Myelosuppression and secondary leukemia *Additional SE: Pulmonary fibrosis |
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Thiotepa
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Alkylating Agent
Electrophiles that react with electron-rich atoms (DNA) in the cells to form covalent cross links which causes inhibition of DNA replication. SE: Myelosuppression and secondary leukemia |
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Mitomycin
|
Antitumor Antibiotics
|
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Cis-platin
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Anti-Neoplastic, Natural Products
MOA: Electrophiles that react with electron-rich atoms (DNA) in the cells to form covalent cross links which causes inhibition of DNA replication. SE: High nausea and nephrotoxicity Important! |
|
Methotrexate
|
Antimetabolite - Folic acid antagonist
MOA: Competitively inhibits dihydrofolate reductase and leads to blockage of tetrahydrofolate synthesis SE: Neutropenia requires *leucovorin rescue. Also leukopenia and thrombocytopenia. Pulmonary pneumonitis. |
|
5-fluorouracil
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Antimetabolite - Pyrimidine Antagonist
MOA: Acts as a false pyrimidine inhibiting the enzyme thymidylate synthase, inhibiting production of thymidine SE: myelosuppression, ulceration of oral and GI muscosa |
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Cytarabine
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Antimetabolite - Pyrimidine Antagonist
AKA cytosine arabinoside MOA: Inhibits DNA polymerase |
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6-mercaptopurine
|
Antimetabolite - Purine Antagonist
MOA: Analogs are incorporated into DNA and also prevent purine synthesis. Requires conversion by the enzyme hypoxanthine guanine- phosphoribosyltransferase *Make sure to genotype for thiopurine methyltransferase. This enzyme breaks down the drug, so if you don't have enough of it, you'll have over-activation of the drug. |
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6-thioguanine
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Antimetabolite - Purine Antagonist
|
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Doxorubicin
|
Antitumor Antibiotics
MOA: Intercalates between base pairs causing DNA breaks, works on S and G2 phases SE: Cardiomyopathies (CHF), discoloration of urine and sweat (red for rubies) |
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Daunorubicin
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Antitumor Antibiotics
MOA: Intercalates between base pairs causing DNA breaks, works on S and G2 phases SE: Cardiomyopathies (CHF), discoloration of urine and sweat (red for rubies) |
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Bleomycin
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Antitumor Antibiotic
MOA: Generates free radicals that fragment DNA. Works on G2 phase. SE: Pulmonary toxicity *Does NOT inhibit bone marrow function Important! |
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Vincristine
|
Antimitotic Drug
MOA: Block polymerization of the mitotic spindle by binding tubulin, works at M phase SE: Neurotoxic *Anything that starts with "vin" is anti-mitotic |
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Vinblastine
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Antimitotic Drug
MOA: Block polymerization of the mitotic spindle by binding tubulin, works at M phase SE: Myelosupression (Blasts the Bone marrow) |
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Paclitaxel
|
Antimitotic Drug
MOA: Promotes the polymerization of microtubules. Overly stable and non-functional SE: Myelosupression (neutropenia DLT), peripheral neuropathy, hypersensitivity |
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Etoposide
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Antineoplastic, Natural products
MOA: Forms a complex with topoisomerase II, forming single stand DNA breaks (Fragment DNA) *Works on S and G2 phases SE: Myelosuppression |
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Camptothecins
|
Antineoplastic, Natural products
*Natural alkaloid found in the bark and wood of Chinese camptotheca tree MOA: Inhibits enzyme topoisomerase I resulting in the stabilization of the cleavage complexes causing reversible single strand DNA breaks. Works on S phase. |
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Hydroxyurea
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Antineoplastic
MOA: Blocks conversion of ribonucleotide --> Deoxyribonucleotide |
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L-asparaginase
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Antineoplastic
MOA: Catalyzes the deamination of asparagine to aspartic acid and ammonia. Tumor cells require external source due to limited capacity to synthesize sufficient amounts. SE: Hypersensitivity |
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Arsenic trioxide
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Antineoplastic
|
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Imantinib
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Tyrosine Kinase Inhibitor
MOA: Inhibits bcr-abl tyrosine kinase activation by occupying the kinase pocket to prevent the phosphorylation of tyrosine SE: Edema, CHF |
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Cetuximab
|
Anti-EGFR antibodies
MOA: Binds to EGFR and inhibits downstream EGFR signaling |
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Trastuzumab
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Anti-EGFR antibodies
MOA: Binds to EGFR and inhibits downstream EGFR signaling *Binds to human epidermal growth factor receptor protein 2 (HER2) inhibiting the proliferation of cells. This is used for breast cancer. |
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Bevacizumab
|
VEGF antibodies
MOA: Inhibits VEGF from stimulating formation of new blood vessels |
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Gefitinib
|
EGFR kinase domain inhibitor
MOA: Inhibits tyrosine kinase domain of EGFR |
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Amantadine
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M2 Inhibitor - Treats Influenza
MOA: Blocks viral membrane matrix protein M2, prevents viral penetration and uncoating. SE: Anticholinergic *Rapid resistance Also used for Parkinson's, CNS SE |
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Rimantadine
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M2 Inhibitor - Treats Influenza
MOA: Blocks viral membrane matrix protein M2, prevents viral penetration and uncoating. SE: Anticholinergic *Rapid resistance |
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Ribavarine
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Antiviral - Treats Hep C
MOA: Inhibits IMP dehydrogenase (interferes with DNA synthesis) SE: Hemolytic anemia and rash Important! |
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Acyclovir
|
Antiviral - Guanosine analog
Treats Herpes - DOC for HSV encephalitis MOA: Guanosine analog that is phosphorylated by thymidine kinase (MUST be activated by this), inhibiting DNA polymerase by chain termination. SE: Nephrotoxic IMPORTANT! |
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Valcyclovir
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Antiviral - Guanosine analog
Treats Herpes *Prodrug for Acyclovir MOA: Guanosine analog that is phosphorylated by thymidine kinase, inhibiting DNA polymerase by chain termination. |
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Penciclovir
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Antiviral - Treats Herpes
MOA: Inhibits viral DNA polymerase *Topical formulation |
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Famciclovir
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Antiviral - Treats Herpes
MOA: Inhibits viral DNA polymerase *Topical formulation |
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Ganciclovir
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Antiviral - Treats Herpes
MOA: Guanosine analog that is phosphorylated by thymidine kinase, inhibiting DNA polymerase by chain termination. DOC: Cytomegalovirus (CMV) SE: Hepatotoxic, nephrotoxic |
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Vidarabine
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Antiviral - Treats Herpes
Topical |
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Trifluridine
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Antiviral - Treats Herpes
Topical |
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Idoxuridine
|
Antiviral - Treats Herpes
MOA: Thymidine analog that inhibits DNA polymerase and incorporated in DNA chain, causing early termination Used topically (too toxic for systemic use) |
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Foscarnet
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Antiviral - Treats Herpes
MOA: Non-nucleoside analog of pyrophosphate that reversibly inhibits viral DNA polymerase SE: Nephrotoxic, chelation *Last line if a lot of virals are resistant |
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Sorivudine
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Antiviral - Treats Herpes
*Discontinued MOA: Guanosine analog that is phosphorylated by thymidine kinase, inhibiting DNA polymerase by chain termination. |
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Retrovir
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NRTI
MOA of NRTIs: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination |
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Didanosine
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NRTI
*A analog MOA of NRTIs: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination SE: Peripheral neuropathy, Pancreatitis Important! |
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Zalcitabine
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NRTI
*C analog MOA of NRTIs: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination SE: Peripheral neuropathy Important! |
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Stavudine
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NRTI
*T analog MOA of NRTIs: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination SE: Peripheral neuropathy Important! |
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Lamivudine
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NRTI
*C analog MOA of NRTIs: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination |
|
Emitricitabine
|
NRTI
*C analog MOA: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination SE: Lactic acidosis |
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Abacavar
|
NRTI
*G analog MOA of NRTIs: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination SE: Lipotrophy, *5% Hypersensitivity (drug fever and rash, malaise, respiratory distress) |
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Tenofovir
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NRTI
MOA of NRTIs: Analogs of nucleosides which lack a 3’-OH group and when incorporated to viral DNA by RT, causes DNA chain termination SE: Lipoatrophy |
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Nevirapine
|
NNRTI
*P450 Inducer MOA of NNRTIs: Bind to RT active site, inducing conformation change. Block RNA/DNA dependent DNA polymerase. SE: Rash!, severe hepatotoxicity Important! |
|
Delavirdine
|
NNRTI
*Inhibits P450 MOA of NNRTIs:Bind to RT active site, inducing conformation change. Block RNA/DNA dependent DNA polymerase. SE: Rash! Important! |
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Efavirenz
|
NNRTI
*P450 Inducer MOA of NNRTIs: Bind to RT active site, inducing conformation change. Block RNA/DNA dependent DNA polymerase. SE: Rash! Important! |
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Saquinavir
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Protease Inhibitor
MOA of PIs: Inhibits HIV protease (cleaves polyprotein into essential enzymes). Prevents protease from processing HIV structural proteins, proteins required for virion assembly, and RT. Makes immature, noninfectious virions. PK of PIs: Potent inhibitors of 3A4 and 2D6 SE: Metabolic problems, fat redistribution (buffalo back) |
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Ritonovir
|
Protease Inhibitor
*Used as booster MOA of PIs: Inhibits HIV protease (cleaves polyprotein into essential enzymes). Prevents protease from processing HIV structural proteins, proteins required for virion assembly, and RT. Makes immature, noninfectious virions. PK of PIs: Potent inhibitors of 3A4 and 2D6 SE: Metabolic problems, fat redistribution (buffalo back) Important! |
|
Indiavir
|
Protease Inhibitor
MOA of PIs: Inhibits HIV protease (cleaves polyprotein into essential enzymes). Prevents protease from processing HIV structural proteins, proteins required for virion assembly, and RT. Makes immature, noninfectious virions. PK of PIs: Potent inhibitors of 3A4 and 2D6 SE: Metabolic problems, fat redistribution (buffalo back) *Causes nephrolithiasis (kidney stones, know this) |
|
Nelfinavir
|
Protease Inhibitor
MOA of PIs: Inhibits HIV protease (cleaves polyprotein into essential enzymes). Prevents protease from processing HIV structural proteins, proteins required for virion assembly, and RT. Makes immature, noninfectious virions. PK of PIs: Potent inhibitors of 3A4 and 2D6 SE: Metabolic problems, fat redistribution (buffalo back) |
|
Amprenavir
|
Protease Inhibitor
MOA of PIs: Inhibits HIV protease (cleaves polyprotein into essential enzymes). Prevents protease from processing HIV structural proteins, proteins required for virion assembly, and RT. Makes immature, noninfectious virions. PK of PIs: Potent inhibitors of 3A4 and 2D6 SE: Metabolic problems, fat redistribution (buffalo back) |
|
Penicillin G/V
|
Natural Penicillins
*Used for strep and syphilis MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan SE: Hypersensitivity (Type1) due to haptens Resistance: B-lactamase Important! |
|
Nafcillin
|
B-lactamase Resistant Penicillin
*Mainly for S. aureus MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan Important! |
|
Oxacillin
|
B-lactamase Resistant Penicillin
*Mainly for S. aureus MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan Important! |
|
Cloxacillin
|
B-lactamase Resistant Penicillin
*Mainly for S. aureus MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan |
|
Dicloxacillin
|
B-lactamase Resistant Penicillin
*Mainly for S. aureus MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan |
|
Ampicillin
|
Aminopenicillin
*Gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan Important! |
|
Amoxacillin
|
Aminopenicillin
*Gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan Important! |
|
Ticarcillin
|
Anti-pseudomonal Penicillin
MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan |
|
Azlocillin
|
Anti-pseudomonal Penicillin
MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan |
|
Pipercillin
|
Anti-pseudomonal Penicillin
MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan Important! |
|
Cefadroxil
|
First Generation Cephalosporin
*Good gram-pos coverage, modest gram-neg MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan fad faz phal! |
|
Cefazolin
|
First Generation Cephalosporin
*Good gram-pos coverage, modest gram-neg MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan fad faz phal! |
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Cephalexin
|
First Generation Cephalosporin
*Good gram-pos coverage, modest gram-neg MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan fad faz phal! |
|
Cefuroxime
|
Second Generation Cephalosporin
*Better Gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan fur fot fox fac! |
|
Cefotetan
|
Second Generation Cephalosporin
*Better Gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan fur fot fox fac! |
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Cefoxitin
|
Second Generation Cephalosporin
*Better Gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan fur fot fox fac! |
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Cefaclor
|
Second Generation Cephalosporin
*Better Gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan fur fot fox fac! |
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Moxalactam
|
Third Generation Cephalosporins
*Broad gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan *Disulfarim Like reaction |
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Cefotaxime
|
Third Generation Cephalosporins
*Broad gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan |
|
Ceftriaxone
|
Third Generation Cephalosporins
*Broad gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan *Does not cover psuedomonas, DOC for gonorrhea IMPORTANT!! |
|
Ceftazidime
|
Third Generation Cephalosporins
*Broad gram-neg coverage MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan *Pseudomonas Important! |
|
Cefepime
|
Fourth Generation Cephalosporin
Broadest coverage - both gram-pos and gram-neg, covers pseudomonas MOA: Irreversibly inhibit cell wall synthesis by binding to penicillin-binding protein (PBP) interfering with cross-linking of peptidoglycan |
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Clavulanic acid
|
B-lactamase Inhibitor
MOA: Irreversibility binds to B-lactamase “Suicide Inhibitor” Important! |
|
Sulbactam
|
B-lactamase Inhibitor
MOA: Irreversibility binds to B-lactamase “Suicide Inhibitor” Important! |
|
Imipenem
|
Carbopenam
*Broadest B-lactam. Covers gram-pos, gram-neg, anerobes SE: Seizures! Important! |
|
Ertapenem
|
Carbopenam
*Broadest B-lactam. Covers gram-pos, gram-neg, anerobes SE: Seizures! *Does not cover pseudomonas |
|
Vancomycin
|
*Gram-pos, DOC for MRSA!
MOA: Inhibits cell wall formation by binding to terminal D-Ala-D-Ala cell wall precursors, preventing polymerization of peptidoglycans SE: Nephrotoxic, red man's syndrome (infuse drug too fast, causes rash, itchiness due to release of histamines) Resistant: Change an alanine to lactate *SUPER IMPORTANT! |
|
Bacitracin
|
MOA: Inhibits cell wall formation by blocking transport of peptidoglycan precursors across cell membrane
*Topical because nephrotoxic |
|
Cycloserine
|
*Used as 2nd line for anti-TB
MOA: Structure analog of D-Ala that inhibits cell wall synthesis |
|
Neomycin
|
Aminoglycoside
MOA: Bacteriocidal - Binds A site of 30S inhibiting initiation complex and misreading of mRNA template SE: Nephrotoxic, Ototoxic, Teratogen (NOT) Resistance: Enzymatic deactivation (alter sidechain) *Topical, used prior to bowel surgery to "clean" |
|
Gentamicin
|
Aminoglycoside
MOA: Bacteriocidal - Binds 30S inhibiting initiation complex and misreading of mRNA template SE: Nephrotoxic, Ototoxic, Teratogen (NOT) Resistance: Enzymatic deactivation (alter sidechain) *Low cost, reliable activity against gram-neg bacilli |
|
Streptomycin
|
Aminoglycoside
MOA: Bacteriocidal - Binds 30S inhibiting initiation complex and misreading of mRNA template SE: Nephrotoxic, Ototoxic, Teratogen (NOT) Resistance: Enzymatic deactivation (alter sidechain) *1st line antiTB - RIPE(S), plague |
|
Amikacin
|
Aminoglycoside
MOA: Bacteriocidal - Binds 30S inhibiting initiation complex and misreading of mRNA template SE: Nephrotoxic, Ototoxic, Teratogen (NOT) Resistance: Enzymatic deactivation (alter sidechain) |
|
Tobramycin
|
Aminoglycoside
MOA: Bacteriocidal - Binds 30S inhibiting initiation complex and misreading of mRNA template SE: Nephrotoxic, Ototoxic, Teratogen (NOT) Resistance: Enzymatic deactivation (alter sidechain) |
|
Kanamycin
|
Aminoglycoside
MOA: Bacteriocidal - Binds 30S inhibiting initiation complex and misreading of mRNA template SE: Nephrotoxic, Ototoxic, Teratogen (NOT) Resistance: Enzymatic deactivation (alter sidechain) |
|
Erythromycin
|
Macrolide
Indications: Atypical pneumonias MOA: Binds to 23S rRNA on 50S inhibiting translocation (slide) of peptide chain SE: GI irritations, **prolonged QT Resistance: Decrease affinity of 50S (modification of 23S rRNA by Erm methylases) |
|
Clindamycin
|
Macrolide
*Covers gram-pos, anaerobes and community MRSA!! Indications: Atypical pneumonias MOA: Binds to 23S rRNA on 50S inhibiting translocation (slide) of peptide chain SE: GI irritations, **prolonged QT, **Pseudomonas colitis! Resistance: Decrease affinity of 50S (modification of 23S rRNA by Erm methylases) *This is the #1 cause of c. diff Important! |
|
Clarithromycin
|
Macrolide
Indications: Atypical pneumonias MOA: Binds to 23S rRNA on 50S inhibiting translocation (slide) of peptide chain SE: GI irritations, **prolonged QT Resistance: Decrease affinity of 50S (modification of 23S rRNA by Erm methylases) *Used in triple treatment of H. pylori! |
|
Azithromycin
|
Macrolide
Indications: Atypical pneumonias MOA: Binds to 23S rRNA on 50S inhibiting translocation (slide) of peptide chain SE: GI irritations, **prolonged QT Resistance: Decrease affinity of 50S (modification of 23S rRNA by Erm methylases) |
|
Chloramphenicol
|
MOA: Blocks peptide formation at 50S
SE: Gray baby syndrome (drug can't be broken down by babies) *Can inhibit mitochondrial ribosomes, causing bone marrow toxicity |
|
Oxytetracycline
|
Tetracycline
MOA: Binds to the 30S and competes with tRNA for the A site SE: GI, chelation in growing children (yellow teeth) CI: Do not use in pregnancy or children less than 8 Resistance: Widespread due to Mg2+ dependent active efflux by plasmid encoded protein TetA |
|
Chlortetracycline
|
Tetracycline
MOA: Binds to the 30S and competes with tRNA for the A site SE: GI, chelation in growing children (yellow teeth) CI: Do not use in pregnancy or children less than 8 Resistance: Widespread due to Mg2+ dependent active efflux by plasmid encoded protein TetA |
|
Doxycycline
|
Tetracycline
MOA: Binds to the 30S and competes with tRNA for the A site SE: GI, chelation in growing children (yellow teeth) CI: Do not use in pregnancy or children less than 8 Resistance: Widespread due to Mg2+ dependent active efflux by plasmid encoded protein TetA *Used to treat malaria Important! |
|
Methacycin
|
Tetracycline
MOA: Binds to the 30S and competes with tRNA for the A site SE: GI, chelation in growing children (yellow teeth) CI: Do not use in pregnancy or children less than 8 Resistance: Widespread due to Mg2+ dependent active efflux by plasmid encoded protein TetA |
|
Minocyclin
|
Tetracycline
MOA: Binds to the 30S and competes with tRNA for the A site SE: GI, chelation in growing children (yellow teeth) CI: Do not use in pregnancy or children less than 8 Resistance: Widespread due to Mg2+ dependent active efflux by plasmid encoded protein TetA |
|
Sulfamethoxazole
|
Sulfonamide
MOA: Bacteriostatic - PABA analog that inhibits dihydropteroate synthase (enzyme that converts dihydropteroid acid --> folate). SE: Hypersensitivity (rash), hemolytic anemia (G6PD) |
|
Sulfisoxazole
|
Sulfonamide
MOA: Bacteriostatic - PABA analog that inhibits dihydropteroate synthase (enzyme that converts dihydropteroid acid --> folate). SE: Hypersensitivity (rash), hemolytic anemia (G6PD) |
|
Sulfadiazine
|
Sulfonamide
MOA: Bacteriostatic - PABA analog that inhibits dihydropteroate synthase (enzyme that converts dihydropteroid acid --> folate). SE: Hypersensitivity (rash), hemolytic anemia (G6PD) |
|
Sulfasalazine
|
Sulfonamide
MOA: Bacteriostatic - PABA analog that inhibits dihydropteroate synthase (enzyme that converts dihydropteroid acid --> folate). SE: Hypersensitivity (rash), hemolytic anemia (G6PD) |
|
Sulfacetamide
|
Sulfonamide
MOA: Bacteriostatic - PABA analog that inhibits dihydropteroate synthase (enzyme that converts dihydropteroid acid --> folate). SE: Hypersensitivity (rash), hemolytic anemia (G6PD) |
|
Sulfadoxine
|
Sulfonamide
MOA: Bacteriostatic - PABA analog that inhibits dihydropteroate synthase (enzyme that converts dihydropteroid acid --> folate). SE: Hypersensitivity (rash), hemolytic anemia (G6PD) *Used to treat malaria! |
|
Trimethoprim
|
MOA: Inhibits bacterial dihydrofolate reductase (enzyme that converts folate --> tetrahydrofolic acid)
SE: Treats marrow poorly (TMP) |
|
Nalidixic acid
|
Quinolone
MOA: Inhibits DNA gyrase (topoisomerase IV) to prevent resealing of DNA, inhibiting cell division PK: Decreases absorption of divalent cations SE: Ruptured tendons! |
|
Norfloxacin
|
Quinolone
MOA: Inhibits DNA gyrase (topoisomerase IV) to prevent resealing of DNA, inhibiting cell division PK: Decreases absorption of divalent cations SE: Ruptured tendons! |
|
Ciprofloxain
|
Quinolone
MOA: Inhibits DNA gyrase (topoisomerase IV) to prevent resealing of DNA, inhibiting cell division PK: Decreases absorption of divalent cations SE: Ruptured tendons! |
|
Isoniazid
|
Antimycobacterial Drug
MOA: Inhibits synthesis of mycolic acids PK: Metabolized by acetylation (slow vs fast) SE: Periphral neuropathy (give vit B6), hepatotoxic *1st line antiTB drug - RIPE(S) Important! |
|
Pyrazinamide
|
Antimycobacterial Drug
MOA: Requires acidic environment to inhibit synthesis of mycolic acids *1st line antiTB drug - RIPE(S) |
|
Rifampin
|
Antimycobacterial Drug
MOA: Inhibits DNA-dependent RNA polymerase PK: Induces P450 SE: Hepatitis, red/orange fluids *1st line antiTB drug - RIPE(S) |
|
Ethambutol
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Antimycobacterial Drug
MOA: Inhibits synthesis of outer coating of cell wall by inhibiting arabinosyl transferase SE: Optic neuritis (Starts with E --> Eyes) *1st line antiTB drug - RIPE(S) |
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Dapsone
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Anti-leprosy
MOA: PABA antagonist to inhibit folate biosynthesis SE: Hemolysis (G6PD) |
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Metronidazole
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Antiprotozoal
DOC for c. diff MOA: Froms cytotoxic compound (ROS) that bind to proteins and DNA DI: Disulfiram-like reaction with alcohol (Can't take with alcohol) IMPORTANT! Take this if you see protozoa. |
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Primaquine
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Treats malaria
SE: Hemolytic anemia (G6DP) |
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Quinine
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Treats malaria
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Chloroquine
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Treats malaria
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Mefloquine
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Treats malaria
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Pyrimethamine
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Treats malaria
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Haloxanthrine
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Treats malaria
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Artemisinin
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Treats malaria
*Derived from Qinghaosu plant *Safe drug! |
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Niridazole
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Trematodes - Flatworms
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Ivermectin
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Nematodes - Roundworms
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Diloxanide furoate
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Luminal amebicide
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Niclosamide
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Cestodes - Tapeworms
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Iodoquinol
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Luminal amebicide
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Praziquantel
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Trematodes/Cestodes - Flatworms/Tapeworms
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Pyrantel Pamoate
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Nematodes - Roundworms
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Piperazine
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Nematodes - Roundworms
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Diethylcarbamazepine
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Nematodes - Roundworms
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Mebendazole
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Bendazole
MOA: interferes with the polymerization/assembly of the parasites’ microtubules, affecting microtubule- dependent uptake of glucose (selective for helminth tubulin) Use bendazoles if you see worms! |
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Thiabendazole
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Bendazole
MOA: interferes with the polymerization/assembly of the parasites’ microtubules, affecting microtubule- dependent uptake of glucose (selective for helminth tubulin) Use bendazoles if you see worms! |
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Albendazole
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Bendazole
MOA: interferes with the polymerization/assembly of the parasites’ microtubules, affecting microtubule- dependent uptake of glucose (selective for helminth tubulin) Use bendazoles if you see worms! |