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126 Cards in this Set
- Front
- Back
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DAY 1:
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back
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What are the peptidoglycan synthesis inhib's?
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Bacitracin
Vancomycin Cycloserine |
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What are the 50s Inhib's?
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"*CCELLS (Buys AT 30 CCELLS at 50)
Chloramphenicol Clindamycin Erythromycin Lincomycin Linezolid Streptogramins |
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What are the Macrolides?
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ACE
Azythromycin Clarithromycin Erythromycin |
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What are the Streptogramins?
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Dalfopristin
Quinopristin |
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What are the 30s Inhib's?
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*AT (Buys AT 30 CCELLS at 50)
AMG's Tetracyclines (doxycycline, demecyocycline, minocycline, tetracycline) |
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What are the AMG's?
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*STANG
Streptomycin Tobramycin Amikacin Neomycin Gentamicin |
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What are the Nucleotide Synthesis Inhib's?
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Sulfonamides
Trimethroprim Pyrimethamine Methotrexate |
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What is the MOA of Sulfonamides?
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Inhibition of Dihydropterate Synthase
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What is the MOA of Trimethoprim?
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Inhibition of Dihydrofolate Reductase
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What is the MOA of Pyrimethamine?
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Inhibition of Dihydrofolate Reductase
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What drugs inhibit DHF Reductase?
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Trimethoprim
Pyrimethamine Methotrexate |
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What blocks DNA Topoisomerase II?
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Quinolones
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What blocks DNA Gyrase?
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Quinolones (DNA Topoisomerate II & DNA Gyrase are the same)
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What blocks mRNA Synthesis
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Rifampin
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How does Rifampin's MOA work?
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Inhibition of DNA-dependent RNA polymerase, thereby blocking mRNA synthesis
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What drugs block bacterial & fungal membranes?
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"Polymixins (Polymixin B & Polymixin E)
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What drugs destroy fungal membranes?
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Amphotericin B
Nystatin |
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What is the MOA of Penicillins?
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1) Bind PBP's
2) Activates autolytic enzymes 3) Inhibits transpeptidase cross-linking |
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What is the end-result of transpeptidase cross-linking?
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Formation of peptide bonds between nucleotides
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What are the peptidoglycan synthesis inhib's?
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Bacitracin
Vancomycin Cycloserine |
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What is the c/u of Penicillins? (1st generation)
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G+ rods & cocci
G- cocci Spriochetes |
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What does Penicillin toxicity cause?
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Hypersensitivity
Hemolytic Anemia |
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What does Methicillin toxicity cause?
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Interstitial nephritis
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What is the c/u for Methicillin?
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Staph Aureus
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What is used for MRSA?
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Vancomycin
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What are the anti-Staph Penicillins?
(Anti-Staph PCN's = 2nd Gen PCN) |
*CONDM
Cloxacillin Oxacillin Nafcillin Dicloxacillin Methicillin |
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What are the anti-Pseudomonas Penicillins?
(4th Gen PCN) |
*PTC of Pseudomonas in the AM
Piperacillin Ticarcillin Carbenicillin Azlocillin Mezlocillin |
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What is the order of tx for Pseudomonas?
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1. AMG's (1st for any G- rod)
2. 3rd Gen Ceph's 3. Anti-Pseudomona PCN's |
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What is the c/u of Ampicillin/Amoxicillin?
(3rd Gen PCN) |
*HELPS Enterococci
H. Influenza E. Coli Listeria Proteus Salmonella Enterococci |
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What is co-administered with Ampicillin/Amoxicillin?
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Clavulonic Acid
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What is the MOA of clavulonic acid?
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Inhibition of Penicillinase (Beta-Lactamase)
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What are the anti-Penicillinase's?
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*CONDM + Ampicillin/Amoxicillin w/Clavulonic Acid + all Cephalosporins
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What are the Penicillinase/B-Lactamase inhibitors?
(these drugs are resistant to B-Lactamases) |
*AIM
Aztreonam Imipenem/Cilistatin Meropenem |
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What is the c/u for the Penicillinase/B-Lactamase inhibitiors?
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"G- bugs
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What does Ampicillin/Amoxicillin toxicity cause?
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Hypersensitivity
Ampicillin rash Pseudomembranous colitis |
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Which antibiotics cause Pseudomembranous Colitis?
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Ampicillin/Amoxicillin
Clindamycin |
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What is the tx for Pseudomembranous Colitis?
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Metronidazole
Vancomycin |
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What are the 50s Inhib's?
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*CCELLS (Buys AT 30 CCELLS at 50)
Chloramphenicol Clindamycin Erythromycin Lincomycin Linezolid Streptogramins |
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What are some 1st Gen Ceph's?
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*Cephalosporin that begin with ""Cefa-"" or ""Cepha-"" prefixes
Cefazolin Cephalexin Exception: Cefaclor is a 2nd Gen Ceph. Only a few 1st Gen Cephs don't start w/one of these 2 prefixes |
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What is the c/u for 1st Gen Ceph's?
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*PEcK (c = cocci)
Proteus E. Coli Klepsiella G+ cocci |
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What are the G+ cocci?
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Staphyloccoci
Streptococci |
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What are some 2nd Gen Ceph's?
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* A FAMily of FOXes has FURry ""TETs""
Cefamandole Cefoitin Cefuroxime Cefotetan Cefaclor (exception to 1st Gen Ceph's rule) |
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What is the c/u for 2nd Gen Ceph's?
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*HEN PEcKS (c = cocci)
H. Influenza Enterobacter Neisseria Proteus E. Coli Klebsiella Serratia (red pigment) G+ cocci |
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What are some 3rd Gen Ceph's?
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Cefixime
Ceftriaxone Ceftazidime Cefotaxime Cefeparazone |
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What is a 3rd Gen Ceph used to tx Pseudomona?
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Ceftazidime
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What is a 3rd Gen Ceph used to tx Gonorrhea?
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Ceftriaxone & Cefixime
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What are the Ceph's that tx Gonorrhea?
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*TRI to FIX a FOX
Ceftriaxone (3rd) Cefixime (3rd) Cefoxitin (2nd) |
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What is the one-dose tx for Chlymdia?
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Azithromycin
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What are the Ceph's that cause a Disulfram-like reaction with Etoh?
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*PAIR of FAMily ""TETS"" (****)
Cefeparazone (3rd) Cefamandole (2nd) Cefotetan (2nd) |
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What are some 4th Gen Ceph's?
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Cefipime
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What is the MOA of Aztreonam?
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*AzTHREEonam
Binds to PBP #3 |
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What is the c/u for Imipenem/Cilastatin?
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DOC for Enterobacter
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What is the MOA of Vancomycin?
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Inhibition of D-ala D-ala
t/f it can't make peptidoglycan |
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What are the peptidoglycan synthesis inhib's?
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Bacitracin
Vancomycin Cycloserine |
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What is the c/u for Vancomycin?
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MRSA
Pseudomembranous Colitis Any nosocomial infection |
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Vancomycin is the tx for Pseudomembranous Colitis 2ndary to what?
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C. Difficile
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Why is Vancomycin used for nosocomial infections?
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"Nosocomial is defined as any infection that is ""picked up"" while hospitalized; it is t/f assumed that it is probably drug-resistent
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What is the tx for VRSA?
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Linezolid
Streptogramins (-pristins) |
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What are the Streptogramins?
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Dalfopristin
Quinopristin |
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What is the MOA of Linezolid?
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Inhibition of 50s
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What is the MOA of Streptogramins?
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Inhibition of 50s
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What is the tx for linezolid-Resistent Staph Aureus?
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Call the clergyman to pray for the pt b/c there is nothing else
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What is the toxicity of Vancomycin?
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*There is NOT toxicity
Neurotoxic Ototoxic Thrombophlebitis |
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What are the Ototoxic-causing drugs?
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AMG's
Loops (Furosemide) Vancomycin Quinidine (Na channel blocker) Chloroquine (malaria) |
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What is the MOA of AMG's?
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Inhibits initiation complex of N-acetyl formation causing misreading of mRNA
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What is the c/u of AMG's?
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G- Rods
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For what are AMG's used 1st line?
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Pseudomonas infections
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What is the tx of Pseudomonas infection in a pt who cannot tolerate AMG's?
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Aztreonam
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What is the c/u of Aztreonam?
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G- rods in pt's who cannot tolerate AMG's
OR Pt's allergic to Penicillin OR Pt's with Renal Failure |
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Why is Aztreonam used in pt's with Renal Failure?
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AMG's are Nephrotoxic
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What is the toxicity of AMG's?
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*There is NNO toxicity
Neurotoxic (teratogenic) Nephrotoxic Ototoxic |
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MOA of Tetracyclines?
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Protein synthesis inhibition by preventing amino acyl tRNA attachment
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What is the function of amino acyl tRNA?
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It "charges" the tRNA molecule
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Why does tRNA need to be charged?
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"Charging" provides "energy" to pick up the next nucleotide
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What is the c/u for Tetracyclines?
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*VACUuM The BR
Vibrio Cholerea Acne (Propionibacterium Acnes) Chlamydia Ureaplasma Urealyticum Mycoplasm Tularemia H. Pylori Borellia Rickettsia |
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What is the toxicity of Tetracyclines?
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Discoloration of teeth (children)
Abnormal bone growth (children) Photosensitivity Drug-induced Hepatitis Fanconi Syndrome (old Tetracyclines) |
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What is the MOA of Macrolides?
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*Inhibits ""Macroslide"" (macro = 50s; slide = translocation)
Blocks translocation from the A-->P site by binding the 23s subunit of the 50s ribosome. |
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What is the enzyme that transfers nucleotides from the A --> P site?
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Peptidyltransferase
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What drug inhibits Peptidyltransferase?
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Chloramphenicol
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What is the MOA of Clindamycin?
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Inhibits peptide bond formation
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Where does the Clindamycin MOA take place?
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The P site
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What part of protein synthesis normally takes place on the P site?
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Single nucleotides are transferred from the A --> P site
Nucleotides begin to accumulate in a line Accumulation ofnucleotides, form a 'growing protein at the P site. |
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Summerize the 3 drugs that have MOA that inhibit the protein synthetic process (prior to its detachment from the ribosome).
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""MCC"" of drug-induced protein synthesis inhibition (not literally; just a mnemonic)
Macrolides: Inhibit 23s subunit of 50s, blocking translocation (A-->P) of nucleotides Chloramphenicol: Inhibits Peptidyltransferase, the enzyme responsible for transferring nucleotides from A-->P site. Clindamycin: Inhibits peptide bond formation b/w nucleotides at the P site |
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What is the c/u of Macrolides?
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*UPS Lost My Brand New Car
URI's (caused by G+ cocci) Pneumonia (cused by G+ cocci) STD's (caused by G+ cocci) Legionella Mycoplasma Bordatella Neisseria Chlamydia |
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What are the SE's of Macrolides?
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Acute Cholestatic Hepatitis
Eosinophilia |
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What is the MOA of Chloramphenicol?
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"Inhibition of Peptidyltransferase, the enzyme responsible for transferring nucleotides from A --> P site
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What is the c/u for Chloramphenicol?
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Bacterial Meningitis
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What is the toxicity of Chloramphenicol?
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Dose-dependent Anemia
Dose-independent Aplastic anemia Grey Baby Syndrome (premature infants) |
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What are the clinical features of Grey Baby Syndrome?
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Be able to recognize--After 2–9 days Chloramphenicol toxicity results in:
Vomiting Ashen gray color of the skin Limp body tone Hypotension (low blood pressure) Cyanosis blue discoloration fo lips and skin Hypothermia Cardiovascular collapse Unforseeable Blindness |
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Which pt's get Grey Baby Syndrome? & Why?
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Premature infants, b/c their liver & kidneys are not yet fully developed
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What is lacking in Grey Baby Syndrome?
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"1. The UDP-glucuronyl transferase enzyme system of infants, especially premature infants, is immature and incapable of metabolizing the excessive drug load.
2. Insufficient renal excretion of the unconjugated drug. |
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What is the MOA of Clindamycin?
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"Inhibition of bond formation between nucleotides at the P site (i.e. stops ""growing peptide"")
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What is the c/u of Clindamycin?
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Anaerobes above the diaphram (e.g. an alcoholic w/ Pneumonia)
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What is the toxicity of Clindamycin?
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Pseudomembranous Colitis
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What is a half-life?
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"The time it takes the body to remove (i.e. ""clear"") 1/2 of the total amt of a drug distributed throughout the body tissues (i.e. Volume of Distribution, Vd)
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How is half-life calculated?
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T1/2 = Vd/Cl x 0.7
T1/2 = "half-life" Vd = Volume of Distribution Cl = Clearance 0.7 = Constant |
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a. If 75% of a drug remains in the body, how many half-lifes have occured?
b. If 50% of a drug remains in the body, how many half-lifes have occurred? c. If 87.5% of a drug remains in the body, how many half-lifes have occurred? d. If 50% of the drug is eliminated from the body, how many half-lifes hae occured? e. If 75% of the drug is eliminated from the body, how many half-lifes have occured? f. If 90% of the drug is eliminated from the body, how many half-lifes have occured?" |
a. < 1 half-life
b. 1 half-life c. <1 half-life d. 1 half-life e. 2 half-lifes f. 3.3 half lifes Memorize Remaining: T1/2 = 3.3-->10% remaining Eliminated: T1/2 = 3.3--> 90% eliminated |
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What is loading dose?
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Initial dose given in order to quickly reach "target" drug level in the body
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What is the Maintenance Dose?
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"The amt of drug administered to ""replace"" the amt of drug that is ""lost"" (i.e. eliminated/cleared), thereby maintiaining ""target"" drug levels in the body
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What is the "target drug level" in the blood called?
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"Css = Plasma concentration of the drug at steady state (i.e. when maintenance dose = elimination)
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What are two extreme examples?"
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Vd (Volume of distribution) = Volume of body tissues that are holding the drug administered
Total Blood Volume ~ 5L (hydrophilic drug with low Vd) Total Body Water ~ 40L (lipophilid drug with high Vd) |
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What is bioavailability?
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"Bioavaliability, f, is the amount actually absorbed and bioavailable (i.e. in the proper usable form or metabolite)
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What must be considered in order to determine the Loading Dose?
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You have to consider three things:
1. Desired Css 2. f--> is RARELY 100%, so LD must be increased to reach the desired Css 3. Vd--> some amount of the drug usually gets distributed somewhere in the body other than in the blood circulation, therefore, LD will have to be increased to reach the desired Css. |
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How is Loading Dose calculated?
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"LD = (Css x Vd) / f
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How is Maintenance Dose calculated?
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"MD = (Css x Cl) / f
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How is Volume of Distribution calculated?
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"Vd = Amount of drug administered / Css @ t = 0
(requires extrapolation; t = time) |
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How is Clearance calculated?
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Cl = Amount eliminated / Css
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What are 3 drugs that undergo zero-order elimination?
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*EPA
Ethanol Phenytoin Aspirin (high dose) |
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What are the Phase II elimination reactions?
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*GAS
Glucoronidation Acetylation Sulfonation |
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What are the Phase I elimination reactions?
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*HOR
Hydrolysis Oxidation Reduction |
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Which Phase (I or II) DON'T geriatric pt's lose?
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Phase II
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Why don't geriatric pt's lose Phase II elimination reactions?
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They lose Phase I first
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Once geriatric pt's have lost Phase I elimination reactions, why don't they then lose Phase II elimination reactions?
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They die
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What question is answered by Phase I drug development?
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Is it safe?
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What question is answered by Phase II drug development?
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Does it work?
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What question is answered by Phase III drug development?
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FDA double-blind study
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What question is answered by Phase IV drug development?
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Post-market surveillance: What SE's exist?
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On a dosage-response curve, what axis are dosage, response, potency, & efficacy?
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Dosage: x-axis
Response: y-axis Potency: x-axis (indirectly) Efficacy: y-axis (indirectly) |
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On a dose-response curve, a drug with increased potency is shifted which direction (right, left, up, or down)?
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Left (inversely related to dosage/x-axis)
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On a dose-response curve, a drug with increased efficacy is shifted which direction (right, left, up, or down)?
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Up (directly related to response/y-axis)
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What is a competitive antagonist?
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A drug that fights for the SAME RECEPTOR SITE as another substance
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What is a noncompetive antagonist?
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"A drug that binds a receptor REGULATORY SITE (i.e. allosteric site) & decreases the affinity of the RECEPTOR SITE for another substance
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What direction does a competitive antagonist shift the efficacy curve (right, left, up, or down)?
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It doesn't: efficacy (Vmax) is not affected
However, potency is decreased (Km is increased) and therefore the POTENCY curve is shifted to the right. |
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What direction does a noncompetitive antagonist shift the potency curve (right, left, up, or down)?
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"It doesn't: potency (Km) is not affected (the drug is just as potent as before, but some receptors are turned off)
However, efficacy (Vmax) is decreased and therefore the EFFICACY curve is shifted downward. |
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In general, what direction will competitive and noncompetitive antagonists shift the dose-response curve?
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*The same direction we read: DOWN & to the RIGHT!
Noncompetitive affects Y-axis: Downward shift Competitive affects X-axis: Right shift (*CXR) |
