ID: Fluoroquinolones, Aminoglycosides, Lincosamides, Tetracycline & Glylcyclines,

Card Set Information

Author:
merazar15
ID:
224683
Filename:
ID: Fluoroquinolones, Aminoglycosides, Lincosamides, Tetracycline & Glylcyclines,
Updated:
2013-06-22 21:33:50
Tags:
ID Fluoroquinolones Aminoglycosides Lincosamides Tetracycline Glylcyclines
Folders:

Description:
Pharm exam
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user merazar15 on FreezingBlue Flashcards. What would you like to do?


  1. Fluoroquinolone drugs:
    • Ciproflocacin (Cipro)  oral and parenteral
    • Levofloxacin (Levaquin) oral and parenteral
    • Moxiflozacin (Avelox) oral and parenteral§  Gemifloxacin (Factive) oral
    • Ofloxacin (Floxin) oral
    • Norfloxacin (Noroxin)  oral
  2. fluoroquinolone MOA:
    • DNA is normally supercoiled.  In this state, it is difficult to separate. 
    • DNA gyrase  (also called topoisomerase II) relaxes supercoiled DNA by cutting it, permiting rotation to occur, and then reattaching it.
    • Fluoroquinolones bind to and inhibit  DNA gyrase in Gram negative bacteria and topoisomerase IV in gram positive bacteria.·        
    •        Effective in both gram – and + bacteria
    • The fluoroquinolones work on DNA gyrase (topoisomerase II) after the cutting stage, preventing reattachment.  This leads to the release of broken DNA segments.
    • Postulated that accumulation of the broken DNA segments leads to bacterial cell death.
    • Fluoroquinolones inhibit topoisomerase IV by preventing the separation of the replicated chromosomal DNA.  This stops cell divison
    • Fortunately, humans have different forms of topoisomerase II and topoisomerase IV
  3. mechanism of resistance:
    • Mutations in the genes encoding for topoisomerase II and IV could lead               to the inability of the fluoroquinolone to inhibit the enzyme
    • Changes (over-expression) of the efflux pumps or porins of the bacteria  could mean the fluoroquinolone cannot accumulate adequate drug levels
  4. fluoroquinolones kinetics:
    • Can enter human cells easily and thus useful in treating intracellular pathogens
    • Well absorbed from the GI tract
    • With the exception of moxifloxacin (Avelox), all other fluoroquinolones excreted renally; thus dosage adjustments needed in renal impairment
  5. spectrum of activity:
    • Good Gram +
    • very good Gram -
    • and some anaerobes
    • Gram + bacteria:
    • Some staphylococcus aureus
    • Streptococcus pyogenes
    • Viridans group streptococci
    • Streptococcus pneumoniae
  6. SE of fluoroquinolones:
    • GI
    • Headache
    • Dizziness
    • Rash
    • Cartilage abnormalities in juvenile animals
    • Achilles tendon rupture
    • QT prolongation
  7. BBW for fluoroquinolones:
    tendon rupture
  8. fluoroquinolone DI:
    • Avoid taking with di- or tri-valent cations (Mg, Fe, Al, Zn, Ca antacids, multivitamins)
    • Separate by 2 to 6 hours, dependent on agent
  9. which are the respiratory fluoroquinolones?
    what type of coverage do they have?
    • gemifloxacin, levofloxacin, and moxifloxacin
    • enhanced gram-positive coverage, including better coverage of S. pneumoniae.
  10. Quinolones are the best choice for:
    avoid:
    •  for complicated UTIs and kidney infections...or if patients can't take TMP/SMX or nitrofurantoin.
    • Avoid moxifloxacin or gemifloxacin...they don't get into the urine. 
    •  avoid quinolones for UNCOMPLICATED urinary tract infections (UTIs) in women.
  11. Ciprofloxacin is often used for ANY UTI. It usually works, but it can cause a lot of:
    • "collateral damage"...by inducing drug-resistant Staph, Pseudomonas, and other strains of bacteria.
    • Use other antibiotics first for uncomplicated UTIs in otherwise healthy women who are not pregnant.
    • Quinolones usually aren't first-line. Save them for complicated UTIs or other serious infections.
  12. Aminoglycoside drugs:
    • Streptomycin - parenteral
    • Gentamicin - parenteral
    • Neomycin (Neo-Fradin) oral
    • Paromomycin oral
    • Tobramycin inhaled (Tobi) oral parenteral
    • Amikacin (Amikin) parenteral
    • Kanamycin  parenteral
  13. aminoglycoside MOA:
    • There are two thoughts of how aminoglycosides work.
    • Aminoglycosides are protein synthesis inhibitors.
    • They irreversibly bind the 30S ribomal subunit.
    • At low concentrations, they cause misreading of the mRNA by ribosomes, leading to synthesis of proteins with incorrect amino acid sequences.
    • At high concentrations, they stop protein synthesis , trapping the ribosomes at the start codon.
    • Accumulation of these abnormal initiation complexes halts translation
    • In summary, Aminoglycosides are rapidly bactericidal.
    • They irreversibly bind to the 30S bacterial ribosome; protein synthesis is thereby inhibited and cell death occurs.
  14. Aminoglycosides have very good activity against:
    Gram negative bacteria
  15. Gram + bacteria aminoglycosides are used against:
    • Staphylococci
    • Streptococci
    • Enterococci
    • Listeria monocytogenes
  16. Paromomycin is used for:
    • parasitic infections
    • (PP!)
  17. neomycin is given for:
    orally as a bowel preps to inhibit intestinal bacteria prior to surgery; not absorbed from the intestine to the systemic circulation
  18. mechanisms of resistance of aminoglycosides:
    • Ribosome alteration
    • Decreased permeability
    • Inactivation by aminoglycoside modifying enzymes
    • Efflux pumps
  19. kinetics of aminoglycosides:
    • Poorly absorbed in GI tract
    • Nephrotoxicity
    • Most common route of administration is IV but Tobi is inhaled
    • Opthalmic and otic drops are also available; also topical (gentamicin)
    • Rapidly excreted by glomerular filtration.  Half-life in normal renal function is 2 hours.
    • In a patient with renal dysfunction, half-life is 30 to 60 hours.   WOW!!! On exam
    • Has a narrow therapeutic index
  20. SE of aminoglycosides:
    • Ototoxicity
    • Nephrotoxicity (5-10%)
    • Major ones: Vestibular toxicity; auditory toxicity;renal toxicity (reversible); neuromuscular toxicity (post-synaptic curare-like action)
    • Others: skin rash; drug induced fever
    • What to look for: Changes in urine output; creatinine; ototoxicity (hearing tests)
  21. dosing for aminoglycosides:
    • Serum levels must be monitored
    • Peak & trough levels help to determine required doses
    • Dosing must be adjusted based on renal function
  22. Lincosamides drugs:
    • Clindamycin (Cleocin)
  23. Lincosamide MOA:
    • Proteins produced from mRNA
    • mRNA contains the sequencing code based on DNA
    • tRNA contains single amino acids and binds to a three base sequence of DNA
    • Ribosomes are the “machinery” bringing the mRNA and tRNA together to assemble amino acids
    • Lincosamides bind the 23S rRNA of the 50S subunit and inhibit peptidyl transferase, which blocks the transfer of the new amino acid onto the chain
  24. Lincosamides-
    bactericidal or bacteriostatic?
    helpful in reducing what?
    • bacteriostatic
    • Most toxins produced from bacteria are proteins.
    • Since lincosamides inhibit protein synthesis, these drugs are particularly helpful in toxin-producing infections.  Examples include necrotizing fasciitis and toxic shock syndrome.
  25. resistance mechanisms for lincosamides:
    • Enzymatic inactivation of the drug
    • Decreased binding due to a change in the ribosomal binding site
    • Efflux pump.  Macrolides are another type of ribosomal inhibitor.  Interestingly, bacteria that have efflux pumps to pump out macrolides do not pump out clindamycin
    • BUT resistance to clindamycin  usually means cross-resistance to macrolides
  26. kinetics of lincosamides:
    • Well absorbed orally
    • Metabolized by liver
    • No adjustment needed for renal impairment
    • Lots of Rxs for Clindamycin from dentists
    • (good penetration of bone)
    • Does not penetrate well into CNS
  27. antimicrobial activity of lincosamides:
    • Good Gram +
    • Most Gram – bacteria are resistant because their outer membranes resist penetration
    • Very good for anaerobes, especially oral anaerobes
    • Can be used in combination with bacteriocidal drugs for severe gram + infections
  28. SE of licosamides:
    • Pseudomembranous colitis (Clostridium difficile colitis). 
    • Antibiotics may change the gut flora.  Clindamycin is the worst offender, killing the normal flora & letting pathogenic bacteria proliferate.  This leads to inflammation of the colon and diarrhea.
    • C. Dificile can be difficult to treat.  Vancomycin or metronidazole are treatment options.
  29. Tetracycline & glylcyclines drugs:
    • tetracycline oral
    • Doxycycline (Adoxa, Doryx; Monodox, Periostat, Oracea; Vibramycin) oral
    • Minocycline (Minocin) oral
    • Demeclocycline (Declomycin) oral
  30. tetracyclines MOA:
    • Tetracyclines are bacteriostatic
    • Tetracyclines bind reversibly to the 16S subunit of the 30S ribosome.
    •       Binds to a unit of the ribosome, blocks the protein. Bacteria needs protein to live
    • This binding weakens the ribosome tRNA interaction, preventing the addition of amino acids to the growing peptide chain
  31. tetracycline resistance:
    • Efflux pumps: drug is pumped out of bacterial cell.  The newer tetracycline, tigecycline, is NOT pumped out
    • Inhibition of tetracycline binding to the bacterial ribosome
    • Inactivation of tetracycline by bacterial enzymes
  32. what is magic mouthwash?
    • Many patients swear by these prescriptions for mouth pain, multiple canker sores, mucositis from chemo, etc.
    • The usual concoction contains equal amounts of viscous lidocaine and diphenhydramine for analgesia...and Maalox or a similar antacid to enhance coating of the ingredients in the mouth
    • You have to write what you want in it
  33. for preventing and treating lyme disease, what are the 3 approaches:
    • -watchful waiting, a single dose of doxycycline, or a longer course of doxycycline   
    • No approach is wrong...because evidence is scant.   
    • Consider doxycycline for patients bitten in an endemic area...especially if the deer tick is attached for 36 hours or more and treatment is started within 72 hours of removal. For adults, give a single dose of doxycycline 200 mg...or possibly 100 mg BID for 10 days. 
    • Early disease. Treat with antibiotics if a patient has recently been in an endemic area...and now has a rash or flu-like illness. Don't rely on serologic testing within about a month of infection...it's too soon for an antibody response.    Give 14 days of doxycycline for most patients...or amoxicillin or cefuroxime for pregnant women or kids under 8. 
    • Late disease. Arthritis and neurologic symptoms can be seen months to a few years after infection.    
    • For arthritis, give doxycycline, cefuroxime, or amoxicillin for 28 days...and repeat once if appropriate. For neurologic symptoms or worsening arthritis, give ceftriaxone IV for 2 to 4 weeks. 
  34. SE of tetracyclines:
    • GI
    • Photosensitivity
    • Liver damage (rare)
    • Kidney damage (rare)
    • Diabetes insipidus (with which tetracycline?) Demeclocycline
    • Superinfection
    • Minocycline:  hyperpigmentation of skin
    • Teeth mottling.  One of the core rings is a potent chelator of metal ions (calcium).  This may lead to discoloration of teeth & deposition in growing bone
  35. what happens if you use tetracycline that was expired?
    likely to cause Fanconi syndrome
  36. CI for tetracyclines:
    • Pregnancy
    • Less than 8 years old
    • Lactation (possibly unsafe)
  37. why is Demeclocycline different?
    and for what purpose?
    • Inhibits the binding of ADH to its receptor.
    • For SIADH: syndrome of inappropriate   anti-diuretic hormone
    • Remember, ADH acts to increase blood pressure & increase body water

What would you like to do?

Home > Flashcards > Print Preview