Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
89 Cards in this Set
- Front
- Back
|
Cyclophosphamide
1) MOA 2) Toxic effects 3) Phases affected |
MOA: Crosslinking agent
- Activated by CYP450 - Loses two Cl ions to have two + charges - + charges complex with DNA causing a "crosslink" - Prevents replication of DNA and synthesis of RNA Toxic Effects - Bone marrow suppression (mainly leukopenia) - Hemorrhagic cystitis - Pulmonary fibrosis - Alopecia - Sterility - Amenorrhea Phases affected All |
|
|
MESNA
1) Use 2) MOA |
Use
- used in conjunction with cyclophosphamide to prevent hemorrhagic cystitis MOA - Inactivates toxic metabolites of cyclophosphamide |
|
|
Cisplatin
1) MOA 2) Toxic effects 3) Phases affected |
MOA: Crosslinking agent
- Loses 2 Cl ions to gain two + charges - Crosslinks DNA Toxic effects - Primarily renal toxicity (prevent by giving with lots of saline) - Hearing loss - Peripheral neuropathy - Hypocalcemia - Hemolytic anemia Phases affected All |
|
|
Methotrexate
1) MOA 2) Toxic effects 3) Phases affected |
MAO: Metabolite analog (Folate)
- Folic acid used to generate nucleic acids - Acts as a folic acid analog that blocks DHFR's conversion of FH2 to FH4 - Cell can't produce pyrimidines, purines and some amino acids, thus DNA, RNA and Protein synthesis are inhibited Toxic effects - Bone marrow suppression (leukopenia and thrombocytopenia) - Oral/GI ulceration - Renal tubular necrosis - Hepatic fibrosis Phases affected - S-Phase ONLY |
|
|
Leucovorin
1) MOA 2) Use |
MOA
- Folic acid analog that can be used by cells to bypass block by Methotrexate Use - Used in cases where the cancer cells can't uptake the Leucovorin (normal cells can always uptake) - Allows normal cells to grow uninhibited, but starves the cancer cells |
|
|
Fluorouracil (5-FU)
1) MOA 2) Toxic effects 3) Phases affected |
MOA: Metabolite analog (Uracil)
- Stops RNA processing in ribosomes - Causes strand breaks after incorporation into DNA Toxic effects - Bone marrow suppression (Leukopenia, Thrombocytopenia, Anemia) - Alopecia, conjunctivitis, dermatitis Phases affected All |
|
|
Paclitaxel (Taxol)
1) MOA 2) Toxic effects 3) Phases affected |
MOA: Inhibitor of mitosis
- Binds to tubulin and alters normal formation of microtubulin and the mitotic spindle Toxic effects - Neutropenia - Bradycardia - Alopecia Phases affected M phase |
|
|
Tamoxifen
1) MOA 2) Toxic effects 3) Risk populations |
MOA
- Binds to estrogen receptor w/ mixed effect - Antiestrogenic on breast - Estrogenic on bone and uterus Toxic effects - Hot flashes - Menstrual irregularities - Skin rashes Risk populations - Elevated risk of endometrial cancer in post-menopausal women because of estrogenic effect on uterus (use Raloxifene instead) Uses - Use in pre-menopausal women for treating ER+ breast cancer |
|
|
Raloxifene
1) MOA 2) Toxic effects 3) Uses |
MOA
- Binds to estrogen receptor w/ mixed effect - Antiestrogenic on breast/uterus - Estrogenic on bone Toxic effects - Fetal toxic Uses - Use in post-menopausal women instead of Tamoxifen for treating ER+ breast cancer |
|
|
Fulvestrant
1) MOA 2) Toxic effects 3) Uses |
MOA
- Estrogen receptor antagonist - Causes down regulation of the estrogen receptor Toxic effects - Nausea - Vomiting - Constipation - Diarrhea - Abdominal pain - Headache - Back pains - Hot flashes Uses - Used as a backup to tamoxifen and letrozole if the patient doesn't respond to them anymore |
|
|
Herceptin
1) MOA 2) Toxic effects 3) Uses |
MOA: Antibody against p185 HER2
- Antibody to p185 HER2 that is expressed on the surface of 25-30% of breast cancer cells Toxic effects - Fever - Nausea - Vomiting - Diarrhea - Dyspnea - Neutropenia - Anemia - 4% of patients have CHF and decreased left ventricular ejection fraction Uses - Used in conjunction with cyclophosphamide and doxorubicin (53% increased response) |
|
|
DES
1) MOA 2) Toxic effects 3) Uses |
MOA
- An estrogen that causes feedback inhibition of LH and FSH production that causes lowering of testicular androgen secretion Toxic effects - Gynecomastia - Impotence Uses - Used to treat prostate cancer |
|
|
Aminoglutethimide
1) MOA 2) Toxic effects 3) Uses |
MOA
- Inhibits the conversion of cholesterol to pregnenolone thus stopping adrenal androgen production Toxic effects - Lethargy - Skin rashes - Ataxia Uses - Used to treat prostate cancer |
|
|
Leuprolide
1) MOA 2) Toxic effects 3) Uses |
MOA
- GnRH superagonist that prevents LH and FSH secretion, thus lowering androgen production Toxic effects - Bone pain - Hot flashes - Gynecomastia - Impotence - Loss of libido - Edema - Thromboembolism Uses - Used to treat prostate cancer |
|
|
Flutamide
1) MOA 2) Toxic effects 3) Uses |
MOA
- Anti-androgen used to block the androgen receptor - Causes the UNWANTED effect of raising FSH, LH and testosterone levels by decreasing feedback inhibition of FSH and LH secretion and should be thus given with leuprolide Toxic effects - Osteoporosis - Gynecomastia - Decreased libido - Hot flashes - Decreased sperm count - Hepatic toxicity Uses - Used to treat prostate cancer |
|
|
Prednisone
1) MOA 2) Toxic effects 3) Uses |
MOA
- A glucocorticoid, binds to glucocorticoid receptor which upregulates caspase transcription leading to apoptosis Toxic effects - Cushingoid features - Sodium retention - Muscle weakness - Decreased glucose tolerance - Osteoporosis - Peptic ulcerations - Acute tumor lysis syndrome Uses - Used to treat Lympholytic anemias - Used to treat Hodkin's disease - Used to treat non-Hodkin's lymphoma |
|
|
Gleevec
1) MOA 2) Toxic effects 3) Uses |
MOA
- Inhibits bcr-Abl and PDGF tyrosine kinases - Substrate of CYP3A4, CYP2C9 and CYP2D6 and may cross react Toxic effects - Generally mild - Nausea - Muscle cramps - Rash - Diarrhea - Swelling - Anemia - Neutropenia - Thrombocytopenia - Possibly teratogenic Uses - Used to treat chronic myelogenous leukemia (CML) |
|
|
TYKERB
1) MOA 2) Toxic effects 3) Uses |
MOA
- Inhibits EGFR and Epidermal growth receptor type 2 (HER2) Toxic effects - Diarrhea - Nausea - Rash - Fatigue - Decrease in left ventricular ejection fraction - Fetal harm Uses - Used in combination therapy for breast cancer |
|
|
Penicillin G/V
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergic reactions - CNS toxicity Uses - Not serious gram-positive infections Mode of administration - Penicillin G - IV/IM (acid labile) - Penicillin V - oral (not acid labile) Mechanisms of resistance - Beta-lactamase enzymes - Down regulation of influx pumps - Up regulation of outward pumps - PBP mutation CNS Effect - Poor |
|
|
Ampicillin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergic reactions Uses - Relatively broad, gram-positive and gram-negative Mode of administration - IV/IM Mechanisms of resistance - Beta-lactamase enzymes - Down regulation of influx pumps - Up regulation of outward pumps - PBP mutation CNS Effect - Good |
|
|
Amoxicillin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal - Long lasting (12 hour half life) Side effects - Allergic reactions Uses - Relatively broad, gram-positive and gram-negative Mode of administration - IV/IM/Oral Mechanisms of resistance - Beta-lactamase enzymes - Down regulation of influx pumps - Up regulation of outward pumps - PBP mutation CNS Effect - Poor |
|
|
Piperacillin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergic reactions Uses - Used for treating problem gram-negative bacteria like Pseudomonas aeruginosa - Generally given with a beta-lactamase inhibitor Mode of administration - IV/IM Mechanisms of resistance - Beta-lactamase enzymes - Down regulation of influx pumps - Up regulation of outward pumps - PBP mutation CNS Effect - Poor |
|
|
Methicillin, Cloxacillin, Dicloxacillin, Oxacillin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal - Beta-lactamase resistant Side effects - Allergic reactions Uses - Used for treating beta-lactamase producing staphylococcal infections Mode of administration - IV/IM/Oral (varied) Mechanisms of resistance - Down regulation of influx pumps - Up regulation of outward pumps - PBP mutation CNS Effect - Poor |
|
|
Cephalexin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergies - Nephrotoxicity Uses - Gram-positive cocci (except enterococci) Mode of administration - Oral Mechanisms of resistance - Beta-lactamases - PBP mutations CNS effect - None Elimination - Kidney |
|
|
Cefaclor
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergies - Nephrotoxicity Uses - Treatment of staphylococci Mode of administration - Oral Mechanisms of resistance - Beta-lactamases - PBP mutations CNS effect - None Elimination - Kidney |
|
|
Cefoxitin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergies - Nephrotoxicity Uses - Treatment of anaerobic bacterial infection (use on B. fragilis) Mode of administration - IV/IM Mechanisms of resistance - Beta-lactamases - PBP mutations CNS effect - None Elimination - Kidney |
|
|
Ceftriaxone
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergies - Nephrotoxicity Uses - Used to treat Gram-positive and gram-negative bacteria - Excellent activity against enterobacteria - Good activity against Pseudomonas aeruginosa - Can treat highly susceptible meningitis Mode of administration - IV/IM Mechanisms of resistance - Beta-lactamases - PBP mutations CNS effect - Good Elimination - Kidney |
|
|
Cefotaxime
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal Side effects - Allergies - Nephrotoxicity Uses - Used to treat Gram-positive and gram-negative bacteria - Excellent activity against enterobacteria - Used to treat meningitis caused by H. influenzae, meningococci and Enterobacteria Mode of administration - IV/IM Mechanisms of resistance - Beta-lactamases - PBP mutations CNS effect - Good Elimination - Kidney |
|
|
Cefepime
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Impairs the development of bacterial cell walls by preventing the formation of cross-links between peptidoglycan strands by inhibiting transpeptidases - Bacterialcidal - Resistant to Beta-lactamases Side effects - Allergies - Nephrotoxicity Uses - Used to treat Gram-positive and gram-negative bacteria - Excellent activity against enterobacteria - Used to treat Pseudomonas (variants that spew Beta-lactamases) - Used to treat meningitis caused by H. influenzae, meningococci and Enterobacteria Mode of administration - IV/IM Mechanisms of resistance - Beta-lactamases - PBP mutations CNS effect - Good Elimination - Kidney |
|
|
Clavulanic acid/Sulbactam/Tazobactam
1) MOA |
MOA
- Beta-lactamase inhibitors - Enhance the activity of Beta-lactamase sensitive penicillins and cephalasporins |
|
|
Streptomycin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination 8) Class |
MOA
- Inhibits bacterial protein synthesis by binding to the 30S subunit of the ribosome (leads to accumulation of abnormal initiation complexes) - Causes misreading of the mRNA template - Bacterialcidal Side effects - Nephrotoxicity - Less than other aminoglycosides - Ototoxicity - More vestibular than auditory - Neuromuscular blockade Uses - Used in combination with penicillins to treat bacterial endocarditis caused by streptococci or enterococci - Used to treat Tularemia, Plague, Brucellosis Mode of administration - IV/IM Mechanisms of resistance - Development of inactivation enzymes - Altered ribosome binding site - Altered aminoglycoside uptake CNS effect - Poor Elimination - Glomerular filtration (99%) Class - Aminoglycoside |
|
|
Gentamicin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination 8) Class |
MOA
- Inhibits bacterial protein synthesis by binding to the 30S subunit of the ribosome (leads to accumulation of abnormal initiation complexes) - Causes misreading of the mRNA template - Bacterialcidal - Can be used in conjunction with penicillins Side effects - Nephrotoxicity - Most nephrotoxic of the aminoglycosides - Ototoxicity - More vestibular than auditory - Neuromuscular blockade Uses - First choice for many gram-negative infections - Used to treat Pseudomonas, Klbesiella and Serratia Mode of administration - IV/IM Mechanisms of resistance - Development of inactivation enzymes - Altered ribosome binding site - Altered aminoglycoside uptake CNS effect - Poor Elimination - Glomerular filtration (99%) Class - Aminoglycoside |
|
|
Tobramycin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination 8) Class |
MOA
- Inhibits bacterial protein synthesis by binding to the 30S subunit of the ribosome (leads to accumulation of abnormal initiation complexes) - Causes misreading of the mRNA template - Bacterialcidal - Can be used in conjunction with penicillins Side effects - Nephrotoxicity - Less toxic than gentamicin - Ototoxicity - Less toxic than gentamicin - Neuromuscular blockade Uses - Has greater effect than gentamicin against Pseudomonas aeruginosa - More expensive than gentamicin Mode of administration - IV/IM Mechanisms of resistance - Development of inactivation enzymes - Altered ribosome binding site - Altered aminoglycoside uptake CNS effect - Poor Elimination - Glomerular filtration (99%) Class - Aminoglycoside |
|
|
Amikacin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination 8) Class |
MOA
- Inhibits bacterial protein synthesis by binding to the 30S subunit of the ribosome (leads to accumulation of abnormal initiation complexes) - Causes misreading of the mRNA template - Bacterialcidal - Can be used in conjunction with penicillins Side effects - Nephrotoxicity - Ototoxicity - Auditory defects more common than vestibular - Neuromuscular blockade Uses - Treat gram-negative bacillary infections resistant to gentamicin - Used to treat Serratia, Proteus, Pseudomonas aeruginosa, Klebsiella, Enterobacter and E. coli - More expensive than gentamicin Mode of administration - IV/IM Mechanisms of resistance - Development of inactivation enzymes - Altered ribosome binding site - Altered aminoglycoside uptake CNS effect - Poor Elimination - Glomerular filtration (99%) Class - Aminoglycoside |
|
|
Tetracyclines
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Uptake is either passive or active - Binds to the 30S ribosome and inhibit tRNA binding, stops protein synthesis - Can NOT be used with penicillins because Tetracyclines stop growth of the cells - Bacteriostatic Side effects - Allergies - GI irritation (NVD) - Give with meal that doesn't contain divalent cations - Phototoxicity - Liver toxicity - Kidney Toxicity - Brown discoloration of teeth - Suprainfections (Staph. entercolitis or Pseudomembraneous colitis Uses - First choice for Rickettsia, Mycoplasma, Chlamydia, Brucellosis, Cholera, Plague, Lyme disease - Second choice for Clostridium, Campylobacter, Leptospira, Actinomyces - Useful for Anaerobic infections as well as aerobic infections Mode of administration - Oral Mechanisms of resistance - R-factor plasmid interferes with active uptake of tetracycline by actively pumping the drug out of the cell CNS effect - Good Elimination - Glomerular filtration - Biotransformation |
|
|
Chloramphenicol
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Inhibits protein synthesis - Uptake is by facilitated diffusion - Binds to the 50 S ribosomal subunit inhibiting the binding of aminoacyl-tRNA - Bacteriostatic to most bacteria, bactericidal to H. influenzae Side effects - Allergies - Reversible anemia from poisoning of mitochondria in the bone marrow - Irreversible aplastic anemia - NVD - Neonatal toxicity - gray baby syndrome (inability of neonates to glucuronidate the chloramphenicol to be excreted) Uses - Because of high toxicity chloramphenicol is used sparingly - Used to treat Typhoid fever, meningitis, abscesses, rocky mountain spotted fever, brucellosis Mode of administration - Oral Mechanisms of resistance - R factor coding for pump that excretes the drug from the bacteria - Increased acetyltransferase causing an acetylation which deactivates chloramphenicol CNS effect - Good Elimination - Biotransformation by liver (90%) |
|
|
Sulfonamides
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Blocks DHF creation from PABA which blocks anything that requires folate as a precursor (purines, thymidine and amino acids) - Bacteriostatic Side effects - Hemolytic anemia (G6PD deficiency especially at risk) - Aplastic anemia (sickle cell patients at risk) - Thrombocytopenia, eosinophilia - Occlusion of the urinary tract by precipitated granules - Allergies - B2 deficiency due to changes in intestinal bacterial flora Uses - Treat UTIs - Treat skin infections in burn patients - In combination with trimethoprim to treat bacterial diarrhea, Nocardia infection, ear infections and PCP in HIV patients Mode of administration - Oral or IV Mechanisms of resistance - Resistance is widespread CNS effect - Poor Elimination - Primarily by kidney |
|
|
Trimethoprim + Sulfamethoxazole
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) CNS Effect 6) Elimination |
MOA
- Sulfamethoxazole inhibits DHF production, Trimethoprim inhibits THF production (the next step - Double suppression of the THF production hits hard Side effects - In folic acid deficient patients, may see megaloblastosis, leukopenia and thrombocytopenia - Allergies - GI problems - UT problems Uses - UTI - gonococci, E. coli, Yersinia, Shigella, PCP in AIDS patients, Methicillin resistant Staph Mode of administration - Oral CNS Effect - Poor Elimination - Primarily by kidney |
|
|
Ciprofloxacin, ofloxacin, levofloxacin, gatifloxacin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Inhibit the ability of topoisomerase II to ligate enzyme linked DNA breaks - Bind to DNA impairing DNA synthesis - Bacteriocital Side effects - Low allergenic potential - Do not use in patients under 18 - Can cause QT elongation Uses - UTI, prostatitis - GI infections (E. coli, Shigella, Campylobacter - Resistant Staph - Respiratory infections Mode of administration - Oral/IV Mechanisms of resistance - Mutations in topoisomerase II or IV CNS effect - Poor Elimination - Primarily by kidney |
|
|
Clarithomycin, azithromycin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Inhibition of protein synthesis by binding to 50S ribosomal subunit - Blocks t-RNA movement from acceptor site to the peptidyl site -Bacteriostatic Side effects - GI intolerance, diarrhea - Reversible hearing loss - Clarithromycin inhibits CYP450 and thus has drug interactions Uses - Most effective against strep - Not effective against gram-negative bacilli - Very effective against Mycobacterium (TB) - Can be used against Chlamydia, H. influenczae and Legionella Mode of administration - Oral/IV Mechanisms of resistance - Increased efflux by pumps - Production of methylase that modifies the ribosome - Increased esterases that hydrolyzes the drug CNS effect - Poor Elimination - Primarily by hepatic excretion |
|
|
Clindamycin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Inhibit protein synthesis by binding to the 50S ribosomal subunit - Bacteriostatic Side effects - Diarrhea - Pseudomembranous colitis (from C. dif) - Skin rashes in AIDS patients Uses - Useful against anaerobic bacterial infection (B. fragilis) - G(+) cocci respond well - Prophylaxis for Toxoplasma gondii - Used to treat PCP with primaquine Mode of administration - Oral/IV Mechanisms of resistance - Methylation of the ribosome blocking drug interaction CNS effect - Poor Elimination - Hepatic excretion |
|
|
Spectinomycin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Binds to the 30S ribosomal subunit blocking protein synthesis Side effects - Few Uses - Used as second line for Gonococcal infection behind penicillin Mode of administration - IM Mechanisms of resistance - Changes in the binding site on the 30S ribosomal subunit CNS effect - Poor Elimination - Primarily by renal excretion |
|
|
Linezolid
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Prevents formation of the 70S ribosome complex by binding to the 50S subunit Side effects - Few Uses - Active against G(+) bacteria - Last resort for MRSA, MRSE and VRE Mode of administration - Oral/IV Mechanisms of resistance - Mutation of the 50S ribosome binding site CNS effect - 70% infiltration Elimination - 80% excreted by kidney |
|
|
Quinupristin/Dalfopristin (Synercid)
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Binds to 50S ribosomal subunit and stops translocation of t-RNA from acceptor to peptidyl site - Bacteriocidal Side effects - Do not use during pregnancy - Inhibits CYP3A4 - causes drug interactions Use - Active against G(+) bacteria - Reserved for treatment of VRE Mode of administration - IV CNS effect - Poor Elimination - Hepatic excretion |
|
|
Vancomycin
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) Mechanisms of resistance 6) CNS Effect 7) Elimination |
MOA
- Inhibits cell wall synthesis by binding to precursor of peptidoglycan (D-alanyl-D-alanine) - Bacteriocidal Side effects - Allergies - Nephrotoxicity Uses - Mainly used against G(+) bacteria - Reserved for treatment of serious methicillin resistant strains (like MRSA) Mode of administration - IV Mechanisms of resistance - Alterations of precursor to peptidoglycan (D-alanyl-D-alanine) CNS effect - Poor Elimination - Primarily kidney excretion |
|
|
Bacitracin/Polymyxins
1) MOA (including cidal vs static) 2) Side effects 3) Uses 4) Mode of administration 5) CNS Effect |
MOA
- Bacitracin inhibits cell wall synthesis - Polymyxins are cationic detergents that affect cell membrane functions - Bacteriocidal Side effects - Serious nephrotoxicities (rare systemic usage) - Can incrase neuromuscular blockade by non-depolarizing muscle relaxants (curare) Uses - Bacitracin is used topically for supurative conjunctivitis - Polymyxins used topically for skin, eye and ear infections including Pseudomonas aeruginosa - Used to treat C. difficile colitis Mode of administration - Primarily Topical - Oral is not absorbed so can be used to treat gut lumen CNS effect - Poor |
|
|
Acyclovir
1) MOA 2) Uses |
MOA
- Guanosine analog that acts as a DNA chain terminator by blocking DNA polymerase after incorperation into DNA - Given as a prodrug that is first phosphorylated by viral thymidine kinase and then phosphorylated by the cell allowing for specificity - Has much higher affinity for viral DNA polymerase than cellular polymerase Uses - Used to treat HSV 1/2 and VZV |
|
|
Gancyclovir
1) MOA 2) Uses |
MOA
- Given as a prodrug - CMV/cellular phosphokinase phosphorylate to monophosphate form - Cellular kinases continue to triphosphate form - CMV DNA polymerase has much higher affinity for triphosphate form than cellular DNA polymerase Uses - Used to treat CMV infections |
|
|
Cidofovir, Adefovir dipivoxil/Tenofovir
1) MOA 2) Uses |
MOA
- Nucleoside analogs that cause DNA chain termination Use - Broad activity against DNA viruses and HIV RT - Cidofovir used to treat CMV retinitis in AIDS patients, also can be used against smallpox - Adefovir dipivoxil used to treat HBV - Tenofovir used to treat HIV infections in combination with other drugs |
|
|
Ribavirin
1) MOA 2) Uses |
MOA
- Guanosine analog - Acts on multiple levels - Favors Th1 CTL response (better for fighting infection) - Inhibits IMP dehydrogenase to deplete GTP - Substrate for viral polymerase and causes chain termination - Acts as a mutagen after being incorperated into the genome Uses - Used to treat HCV along with INF-alpha - Used to treat influenza and RSV |
|
|
Enfuvirtide
1) MOA 2) Uses |
MOA
- Prevents fusion of HIV envelope to cell membrane by binding to gp41 Uses - Combination therapy of HIV |
|
|
Amantadine, Rimantadine
1) MOA 2) Uses 3) Mechanisms of resistance |
MOA
- Blocks M2 channel of Influenza A virus blocking H+ movement into virus - Without H+, transcription complex is not released Uses - Used to treat Influenza A Mechanisms of resistance - Mutations in the M2 channel |
|
|
Zanamivir, Oseltamivir
1) MOA 2) Uses 3) Mode of administration 4) Mechanisms of resistance |
MOA
- Bind to and plug the active site of the inluenza virus neuraminidase - Blocks the release of Influenza A and B virions from cell surface Mode of administration - Oral or aerosol Mechanisms of resistance - Very little resistance because most mutations of neuraminidase is lethal to the virus |
|
|
Interferon
1) MOA 2) Uses |
MOA
- Upregulates cellular anti-virus mechanisms Uses - Non-specific anti-virus - Used to treat HCV |
|
|
Isoniazid
1) MOA (cidal vs. static as well) 2) Uses 3) Side effects 4) Mechanisms of resistance 5) CNS effect |
MOA
- Inhibits synthesis of mycolic acid (Inhibits fatty acid synthase 2) - Bacteriocidal for growing mycobacteria and bacteriostatic for resting mycobacteria Uses - First line treatment for M. tuberculosis and M. kansasii Side effects - Peripheral neuritis because Isoniazid causes excretion of pyridoxine (B6), prevent by giving pyridoxine with treatment - Hepatic injury, rate of injury increases with age Mechanisms of resistance - Mutation of the catalase-peroxidase CNS effect - Good |
|
|
Rifampin, Rifabutin
1) MOA (cidal vs. static as well) 2) Uses 3) Side effects 4) Mechanisms of resistance 5) CNS effect |
MOA
- Inhibit DNA dependent RNA polymerase - Blocks initiation of the RNA chain Uses - First line drug for M. tuberculosis, M. Kansasii, M. avium complex, M. leprae and M. marinum - Effective against G(+) and G(-) organisms - Bacteriocidal Side effects - Generally well tolerated (alone) - Rifampin is a potent inducer of CYP3A4 and other CYP450s (Rifabutin is not) Mechanisms of resistance - Mutations in DNA dependent RNA polymerase CNS effect - Good |
|
|
Ethambutol
1) MOA (cidal vs. static as well) 2) Uses 3) Side effects 4) CNS effect |
MOA
- Inhibits incorporation of mycolic acid into cell wall - Bacteriostatic Uses - First line drug for M. tuberculosis, M. kansasii, M. avium complex and M. marinum Side effects - Generally mild - Optical neuritis - not used under 5yo -Inhibits excretion of uric acid and can lead to gout CNS effect - Poor |
|
|
Pyrazinamide
1) MOA (cidal vs. static as well) 2) Uses 3) Side effects 4) CNS effect |
MOA
- Inhibits mycolic acid synthesis (Inhibits fatty acid synthase 1) - Bacteriocidal Uses - First line drug for M. Tuberculosis Side effects - Hepatotoxicity CNS effect - Good |
|
|
Clofazimine
1) MOA (cidal vs. static as well) 2) Uses 3) Side effects |
MOA
- Binds to DNA and inhibits template function of DNA - Bacteriocidal Uses - First line drug for M. leprae Side effects - Dry skin, abdominal pain, DVN - Pink to brownish-black discoloration of skin, cornea, retina and urine - Do not use during pregnancy - Absorption can be decreased by Al-Mg antacid |
|
|
Dapsone
1) MOA (cidal vs. static as well) 2) Uses 3) Side effects |
MOA
- Inhibits dihydropteroate synthase, blocking production of THF - Bacteriostatic Uses - First line drug for M. leprae Side effects - Anorexia and nausea - Hemolysis is dose dependant - Allergy - Sulfone syndrome - Rifampin decreases concentration of drug - Primaquine increases risk of hemolysis in G6PD deficient patients - Decreases effectiveness of oral contraceptives |
|
|
Tinidazole
1) MOA 2) Side effects 3) Uses 4) CNS effect |
MOA
- Free radical formation leading to cell destruction Side effects - Generally well tolerated - Metabolized by CYP3A4 (possible drug interactions) Uses - Drug of choice for trichomoniasis, giardiasis and systemic E. histolytica CNS effect - Good |
|
|
Paromomycin
1) MOA 2) Side effects 3) Uses |
MOA
- Inhibits protein synthesis by binding to 30S subunit of ribosome Side effects - Generally mild Uses - Drug of choice for luminal amebiasis |
|
|
Suramin
1) MOA 2) Side effects 3) Uses 4) CNS effect |
MOA
- Disrupts energy metabolism Side effects - Significant toxicity - Including urticaria, photophobia and peripheral neuropathy Uses - Drug of choice against African trypanosomiasis before CNS involvement CNS effect - Poor |
|
|
Pentamidine
1) MOA 2) Side effects 3) Uses 4) CNS effect |
MOA
- Concentrated in parasite via novel purine transporter - Functions by binding to DNA or inhibiting topoisomerase II Side effects - Fairly toxic - Destroys Beta-Islet cells Uses - Used in conjunction with Suramin to treat T.b. gambiense infections, NOT effective against T.b. rhodesiense infections CNS effect - Poor |
|
|
Melarsoprol
1) MOA 2) Side effects 3) Uses 4) Resistance 5) CNS effect |
MOA
- Interacts with sulfhydryl groups inactivating many enzymes - Selective for trypanosomes over mammalian cells Side effects - Encephalopathy (10-12% of patients) - Hemolytic anemia in patients with G6PD deficiency Uses - Drug of choice for African trypanosomiasis with CNS involvement Resistance - T.b. rhodesiense does not gain resistance normally, T.b. gambiense does CNS effects - Good |
|
|
Eflornithine
1) MOA 2) Side effects 3) Uses |
MOA
- Inhibits ornithine decarboxylase Side effects - Anemia, leukopenia Uses - Alternate drug for treatment of CNS involved trypanosomiasis caused by T.b. gambiense - NOT active against T.b. rhodesiense |
|
|
Nifurtimox
1) MOA 2) Side effects 3) Uses |
MOA
- Produces oxygen radicals that kill the parasite - Parasite lacks enzymes that humans have to deactivate the drug Side effects - Insomnia, dementia and seizures - Exacerbated by alcohol Uses - Drug of choice for Chagas disease - No treatment for chronic Chagas disease |
|
|
Sodium stibogluconate
1) MOA 2) Side effects 3) Uses |
MOA
- Decreases fatty acid oxidation and glycolysis Side effects - Not major Uses - Drug of choice for all forms of leishmaniasis |
|
|
Chloroquine
1) MOA 2) Side effects 3) Uses |
MOA
- Accumulates in food vacuoles of malarial parasites - Inhibits heme polymerization causing lysis of the parasite Side effects - Skin eruptions - Alopecia - Exfoliate dermatoses Uses - Drug of choice against erythrocytic phase of malaria |
|
|
Mefloquine
1) MOA 2) Side effects 3) Uses |
MOA
- Accumulated in malaria food vacuole - Mechanism unknown Side effects - CNS dysfunction (psychiatric neurosis) - Possibly teratogenic Uses - Used to treat resistant strains of P. falciparum |
|
|
Pyrimethamine and sulfadoxine
1) MOA 2) Side effects 3) Uses |
MOA
- Pyrimethamine blocks DHF->THF - Sulfadoxine blocks DHF production Side effects - Folic acid deficiency Uses - Used to treat chloroquine resistant P. falciparum |
|
|
Atovaquone and proguanil
1) MOA 2) Uses |
MOA
- Atovaquone inhibits parasite mitochondrial electron transport - Proguanil blocks DHF->THF synthesis Uses - Used to treat RBC stage malaria |
|
|
Primaquine
1) MOA 2) Side effects 3) Uses |
MOA
- Unknown Side effects - Hemolytic anemia in patients with G6PD deficiency Uses - Prevents relapses of malaria by eradicating parasites present in the liver |
|
|
Mebendazole
1) MOA 2) Uses |
MOA
- Inhibits uptake of glucose and uncouples oxidative phosphorylation - Binds Beta-tubulin and blocks microtubule polymerization - Immobilizes parasite Uses - Broad spectrum antihelminthic - Drug of choice against T. trichiura, A. duodenale, N. americanus, A. lumbricoides |
|
|
Albendazole
1) MOA 2) Uses |
MOA
- Inhibits uptake of glucose and uncouples oxidative phosphorylation - Binds Beta-tubulin and blocks microtubule polymerization - Immobilizes parasite Uses - Broad spectrum antihelminthic - Drug of choice against T. spiralis, A. duodenale, N. americanus, A. lumbricoides - ****Cysticercosis**** |
|
|
Pyrantel pamoate
1) MOA 2) Uses |
MOA
- Agonist of NACh receptors - depolarizing neuromuscular blocking agent - Paralyzes worms and induces gut peristalsis Uses - E. vermicularis |
|
|
Diethyl carbamizine
1) MOA 2) Uses |
MOA
- Makes parasites more sensitive to phagocytosis Uses - W. bancrofti (typically given with albendazole) |
|
|
Praziquantel
1) MOA 2) Uses 3) Other |
MOA
- Increases parasite membrane permeability to Ca+2 causing severe muscular contraction - Kills schistosomes - Dislodges cestodes Uses - S. haematobium, S. mansoni, S. japonicum - C. sinensis, P. westermani, T.saginata, D. latum, H. nana - Do NOT use for T. solium because of cysticercosis Other - Metabolized by CYP450 |
|
|
Ivermectin
1) MOA 2) Uses |
MOA
- Activates glutamate-gated and GABA gated Cl- channels causing paralysis of muscles Uses - O. Volvulus - S. stercoralis - W. bancrofti (given with albendazole) |
|
|
Griseofulvin
1) MOA 2) Mode of administration 3) Target fungi |
MOA
- Makes keratin resistant to fungal growth Mode of administration - Oral Target fungi - Ringworm (dermatophytes) |
|
|
Ketoconazole
1) MOA 2) Mode of administration 3) Target fungi |
MOA
- Blocks biosynthesis of fungal lipids Mode of administration - Oral Target fungi - Ringworm (dermatophytes) - Histoplasmosis - Blastomycosis - Coccidioidomycosis - Paracoccidioidomycosis |
|
|
Fluconazole
1) MOA 2) Mode of administration 3) Target fungi |
MOA
- Blocks biosynthesis of fungal lipids Mode of administration - Oral Target fungi - Candidiasis (if superficial) |
|
|
Nystatin
1) MOA 2) Mode of administration 3) Target fungi |
MOA
- Binds firmly to ergosterol allowing a pore to form destroying membrane integrity Mode of administration - Topical Target fungi - Candidiasis |
|
|
Amphotericin B
1) MOA 2) Mode of administration 3) Target fungi |
MOA
- Binds firmly to ergosterol allowing a pore to form destroying membrane integrity Mode of administration - Oral/IV Target fungi - Coccidioidomycosis (with CNS involvement) - Aspergilosis - Candidiasis - Cryptococcosis - Zygomycosis |
|
|
Flucytosine
1) MOA 2) Mode of administration 3) Target fungi |
MOA
- Inhibits thymidylate synthase and DNA synthesis Mode of administration - Oral Target fungi - Candidiasis - Cryptococcosis |
|
|
Bleomycin
1) MOA 2) Side effects 3) Phases affected |
MOA
- Intercalates between DNA strands and causes DNA cleavage via free radicals Side effects - Pulmonary toxicity Phases affected - M or G2 |
|
|
Doxorubicin
1) MOA 2) Side effects 3) Uses 4) Phases affected |
MOA
- Intercalates between DNA and freezes topoisomerase II resulting in strand breaks Side effects - Bone marrow suppression - Cardiac toxicity Phases affected - All |
|
|
Mercaptopurine
1) MOA 2) Side effects 3) Phases affected |
MOA
- Purine analog, incorporated into DNA causing breaks and inhibition of RNA synthesis Side effects - Bone marrow suppression - Hepatotoxicity Phases affected - S-Phase |
|
|
Letrozole
1) MOA 2) Side effects 3) Uses |
MOA
- Lowers estrogen levels by inhibiting aromatase levels Side effects - Fetal toxic Uses - Used as drug of choice in post-menopausal ER+ patients |
