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148 Cards in this Set

  • Front
  • Back
Nystatin
Antifungal

MOA: Bind to ergosterol in plasma membrane to form pores; K+ leakage
*More toxic than amphotericin B
Amphotericin B
Antifungal

MOA: Bind to ergosterol in plasma membrane to form pores; K+ leakage
SE: Renal toxicity, fever and chills
Miconazole
Antifungal - Azole

Topical
PK: Inhibits P450 (3A4)
MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability
SE: Hepatitis
Ketoconazole
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!
Clotrimazole
Antifungal - Azole

Topical
PK: Inhibits P450 (3A4)
MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability
SE: Hepatitis
Fluconazole
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
Itraconazole
Antifungal - Azole

PK: Inhibits P450 (3A4)
MOA: Prevent conversion of lanosterol --> ergosterol. This causes an increase in membrane fluidity and permeability
SE: Hepatitis
Caspofungin
Antifungal

MOA: Inhibit synthesis of fungal cell wall, inhibit synthesis of B-1,3-D- glucan

Important!
Flucytosine
Antifungal


MOA: Cytosine deaminase converts flucytosine to 5-flurodeoxyuridine (5-FU, a false analog) inhibiting thymidylate synthase.
Griseofulvin
Antifungal

MOA: Binds to microtubules to inhibit mitosis
PK: Induces P450
SE: Hepatitis
Mechlorethamine
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
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!
Melphalan
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
bis-chloroethyl nitrosourea (BCNU)
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
Busulfan
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
Thiotepa
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
Mitomycin
Antitumor Antibiotics
Cis-platin
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
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
Cytarabine
Antimetabolite - Pyrimidine Antagonist

AKA cytosine arabinoside
MOA: Inhibits DNA polymerase
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.
6-thioguanine
Antimetabolite - Purine Antagonist
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)
Daunorubicin
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)
Bleomycin
Antitumor Antibiotic

MOA: Generates free radicals that fragment DNA. Works on G2 phase.
SE: Pulmonary toxicity
*Does NOT inhibit bone marrow function

Important!
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
Vinblastine
Antimitotic Drug

MOA: Block polymerization of the mitotic spindle by binding tubulin, works at M phase
SE: Myelosupression (Blasts the Bone marrow)
Paclitaxel
Antimitotic Drug

MOA: Promotes the polymerization of microtubules. Overly stable and non-functional
SE: Myelosupression (neutropenia DLT), peripheral neuropathy, hypersensitivity
Etoposide
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
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.
Hydroxyurea
Antineoplastic

MOA: Blocks conversion of ribonucleotide --> Deoxyribonucleotide
L-asparaginase
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
Arsenic trioxide
Antineoplastic
Imantinib
Tyrosine Kinase Inhibitor

MOA: Inhibits bcr-abl tyrosine kinase activation by occupying the kinase pocket to prevent the phosphorylation of tyrosine
SE: Edema, CHF
Cetuximab
Anti-EGFR antibodies

MOA: Binds to EGFR and inhibits downstream
EGFR signaling
Trastuzumab
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.
Bevacizumab
VEGF antibodies

MOA: Inhibits VEGF from stimulating formation of
new blood vessels
Gefitinib
EGFR kinase domain inhibitor

MOA: Inhibits tyrosine kinase domain of EGFR
Amantadine
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
Rimantadine
M2 Inhibitor - Treats Influenza

MOA: Blocks viral membrane matrix protein M2, prevents
viral penetration and uncoating.
SE: Anticholinergic
*Rapid resistance
Ribavarine
Antiviral - Treats Hep C

MOA: Inhibits IMP dehydrogenase (interferes with DNA synthesis)
SE: Hemolytic anemia and rash

Important!
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!
Valcyclovir
Antiviral - Guanosine analog

Treats Herpes
*Prodrug for Acyclovir
MOA: Guanosine analog that is phosphorylated by thymidine kinase, inhibiting DNA polymerase by chain termination.
Penciclovir
Antiviral - Treats Herpes

MOA: Inhibits viral DNA polymerase
*Topical formulation
Famciclovir
Antiviral - Treats Herpes

MOA: Inhibits viral DNA polymerase
*Topical formulation
Ganciclovir
Antiviral - Treats Herpes

MOA: Guanosine analog that is phosphorylated by thymidine kinase, inhibiting DNA polymerase by chain termination.
DOC: Cytomegalovirus (CMV)
SE: Hepatotoxic, nephrotoxic
Vidarabine
Antiviral - Treats Herpes

Topical
Trifluridine
Antiviral - Treats Herpes

Topical
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)
Foscarnet
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
Sorivudine
Antiviral - Treats Herpes

*Discontinued
MOA: Guanosine analog that is phosphorylated by thymidine kinase, inhibiting DNA polymerase by chain termination.
Retrovir
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
Didanosine
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!
Zalcitabine
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!
Stavudine
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!
Lamivudine
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
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)
Tenofovir
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
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!
Efavirenz
NNRTI

*P450 Inducer
MOA of NNRTIs: Bind to RT active site, inducing conformation change. Block RNA/DNA dependent DNA polymerase.
SE: Rash!

Important!
Saquinavir
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)
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!
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!
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!
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!
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
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
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
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)
Dapsone
Anti-leprosy

MOA: PABA antagonist to inhibit folate biosynthesis
SE: Hemolysis (G6PD)
Metronidazole
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.
Primaquine
Treats malaria

SE: Hemolytic anemia (G6DP)
Quinine
Treats malaria
Chloroquine
Treats malaria
Mefloquine
Treats malaria
Pyrimethamine
Treats malaria
Haloxanthrine
Treats malaria
Artemisinin
Treats malaria

*Derived from Qinghaosu plant
*Safe drug!
Niridazole
Trematodes - Flatworms
Ivermectin
Nematodes - Roundworms
Diloxanide furoate
Luminal amebicide
Niclosamide
Cestodes - Tapeworms
Iodoquinol
Luminal amebicide
Praziquantel
Trematodes/Cestodes - Flatworms/Tapeworms
Pyrantel Pamoate
Nematodes - Roundworms
Piperazine
Nematodes - Roundworms
Diethylcarbamazepine
Nematodes - Roundworms
Mebendazole
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!
Thiabendazole
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!
Albendazole
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!