ID: penicillins, cephalosporins, carapenems, glycopeptides,

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ID: penicillins, cephalosporins, carapenems, glycopeptides,
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2013-06-22 20:14:11
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ID pharm penicillins cephalosporins carapenems glycopeptides
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pharm exam
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  1. Antimicrobial drugs can target:
    • 1) the bacterial cell envelope
    • 2)  their biosynthetic processes
    • 3)  their ability to replicate
  2. describe the structure of gram + bacteria:
    • have a Thick peptidoglycan layer, (structure that makes up the cell wall). 
    • Thus they are more sensitive to β-lactams, antibiotics that act on the cell wall.
    • Human cells don’t have these thick walls! So this is how we target gram positive bacteria
  3. describe the structure of the cell wall:
    • Made up of peptidoglycans, consisting of long sugar polymers, repeating units of two sugars. 
    • Peptides side chains extend from the sugars, creating cross links & making the cell wall stronger.  This cross linking is due to the action of bacterial enzymes, called transpeptidases
  4. Gram + bacteria & infections that they cause:
    • Streptococcus pyogenes:  skin & soft tissue; pharyngitis
    • Streptococcus pneumonia:  sinusitis, otitis media, meningitis, community acquired pneumonia
    • Staphylococcus aureus:  pneumonia, endocarditis, skin & soft tissue, osteomyelitis
    • Enterococcal infections:  wound, intra-abdominal, endocarditis, UTI
  5. Gram - bacteria & infections they cause:
    • Enterobacteriaceae: hospital acquired pneumonia, wound, intra-abdominal, UTI
    • Pseudomonas aeruginosa:  Hospital acquired pneumonia, wounds, UTIs
    • Neisseria:  meningitis, skin & joint, genitourinary
    • Haemophilus influenzae:  otitis media, sinusitis, community acquired pneumonia, meningitis
  6. class of penicillin:
    essential core of penicillin is a:
    • B-lactam
    • four-member ring called a β-lactam ring
  7. penicillin MOA:
    • Bind to the penicillin-binding proteins (PBPs) that normally function to assemble the peptidoglycan cell wall. 
    • This leads to destruction of the bacterial cell wall.
    • (bind and destroy)
    • Normally a new subunit is linked in the peptidoglycan chain.
    • Penicillin binding proteins (PBP) are required for this linking.
    • The beta lactam drug binds the PBP & prevents it from cross linking chains so the glycine (G) bridge is disrupted
    • Inhibit the transpeptidase so it can’t cross-link
  8. what causes bacteria to have different sensitivities?
    • Almost all bacteria have PBPs. (penicilliln binding proteins)
    • Different bacteria have different amounts & different types of PBPs (ex Coli has 7 types & S. aureus 4)
    • Different PBPs have different affinities for  β-lactams; therefore, different bacteria will have different sensitivitities
  9. penicillin SE:
    • N/V/D, abdominal pain, rash
    • An estimated 3-10% of population is allergic.
    • Serious reactions also include hepatotoxicity, seizures, nephritis, pseudomembranous colitis and hematologic abnormalities.
    • Anaphylaxis is rare but life threatening
  10. CI to penicillin:
    • hypersensitivity to drug or class. 
    • Cross reactivity between penicillin allergy & other
    • β-lactam antibiotics is between 1-10%
  11. DI of penicillin:
    • Probenecid.
    •         Competes at the proximal tubule with pen at the kidney. Kidneys will keep penicillin and kick out Probenecid. Combination may increase penicillin levels & extend duration of action.  Increase [] of penicillin
  12. Since nearly all bacteria have cell walls, penicillins should have:
    what type of resistance is a problem with the natural penicillins?
    • broad spectrum of activity
    • intrinsic & acquired resistance
  13. reasons for resistance to natural penicillins:
    • Penetration:  Natural penicillins penetrate poorly into intracellular compartment of human cells.
    • Porins:  Some Gram- bacteria have porins in their outer membrane that don’t allow passage of the natural penicillins
    • Pumps:  Some Gram- bacteria have pumps that do not allow accumulation of the natural penicillins.
    • Penicillinases:  Many bacteria (Gram + and -) make enzymes that degrade natural penicillin· 
    • Some bacteria don’t make peptidoglycan· 
    • Some bacteria make PBPs that natural penicillins don’t bind well
  14. what type of bacteria does penicillin work best on?
    • gram +
    • use for strep throat
  15. penicillin drugs:
    • amoxicillin
    • Augmentin (amoxicillin/Clavulanate)
    • Penicillin VK
  16. dose and indication for amoxicillin:
    Infections, bacterial 500-875 mg PO q 12ho   Vary by infection type/severity
  17. dose and indication for Augmentin:
    • infections, bacterial [500 mg/125 mg-875 mg/125 mg PO q12h]
    • Take with food
  18. dose and indication for penVK:
    • pharyngitis, streptococcal [500 mg PO bid x10 days]·        
    • Take 1h before or 2h after meals (empty stomach)
  19. what are the narrow spectrum penicillins?
    • Dicloxacillin
    • Ocacillin
    • Nafcillin
    • The narrow spectrum penicillins have a bulky side chain that prevents binding of some staphylococcal β-lactamases.
    • Unfortunately, these drugs are NOT able to bind the penicillin binding proteins of methicillin resistant S. aureus (MRSA) or S. epidermidis (MRSE)
    • This group is generally used only to treat certain staphylococcal infections.
  20. what are the aminopenicillins and what are they used for?
    • Ampicillin and Amoxicillin
    • Used for: Otitis Media
  21. what are the β-Lactamase Inhibitor Combinations used for?
    Used to expand the spectrum of the aminopenicillins
  22. what are the extended spectrum penicilins?
    • paracillin & Ticarcillin
    • The side chain of these penicillins is further modified to allow greater penetration into Gram negative bacteria. 
    • They also have increased resistance to the  β-lactamases.
    • Relative to the aminopenicillins (do you remember what these are?), these drugs have better coverage for Gram- negative bacilli including Pseudomonas aeruginosa.
  23. What could you do to make the extended spectrum penicillins even better?
    • AddBeta lactamase inhibitor:
    •      Piperacillin-tazobactam (zosyn) IV
    •      Ticarcillin-clavulanate )Timentin) IV
    •             Zosyn:  Hospital acquired pneumonia: multi-drug resistance likely (for severe infections)
  24. Each generations of the Cephalosporins are:
    effective against a broader range of aerobic Gram - bacteria
  25. what is the structural advantage of cephalosporins vs penicillin?
    • adv: cephalosporins have 2 sites (R and X site) that can be modified
    • also, Bacteriocidal with similar actions to penicillins.   Also have a β-lactam ring
    • intrinsically more resistant to cleavage by β-lactamases
  26. MOA of the cephalosporins:
    • All β-lactams have a similar mechanism of action.
    • Two components needed for β-lactam activity:
    • 1. must bind to penicillin binding protein
    • 2. destruction of bacterial cell wall
  27. 1st generation drugs:
    • Cefadroxil (Duricef);
    • cefazolin* sodium (Ancef, Kefzol),
    • cephalexin (Keflex);
  28. 2nd generation drugs:
    • Cefaclor (Ceclor);
    • cefuroxime (Ceftin, Zinacef (IV,IM));
    • cefprozil (Cefzil);
    • cefoxitin *;
    • cefotetan*;
  29. 3rd generation drugs:
    • Cefdinir (Omnicef);
    • Ceftibuten (Cedax);
    • cefditoren (Spectracef);
    • cefotaxime (Claforan)*;
    • cefixime (Suprax);
    • cefpodoxime (Vantin);
    • ceftriaxone *(Rocephin);
    • ceftazidime*(Fortaz,Tazicef)
  30. 4th generation drugs:
    Cefepime (Maxipime) IM,IV
  31. 5th generation drugs:
    • Ceftaroline (Teflaro) IV
  32. cephalosporins SE:
    • Rarely can cause immediate hypersensitivity reactions including rash, urticaria or anaphylaxis.  Cross-reactivity of between 1-10% with penicillin allergy.
    • Anaphylaxis  due to penicillins is an absolute contraindication for cephalosporin use.
    • Other rare  adverse effects include hematologic effects, Pseudomembranous colitis, nephrotoxicity
    • Diarrhea, nausea, vomiting, rash, elevated liver enzymes may also occur.
  33. what is a DI of cefotetan?
    • Cefotetan and ethanol can lead to a disulfiram-like reaction due to the difference in side chain group
    •        Pt should be warned: DO NOT DRINK ON THIS MED
  34. 1st gen cephalosporins microbial spectrum.
    gram + bacteria:
    gram - bacteria:
    • +: streptococcus pyogenes
    • some viridans streptococci
    • some staphylococcus aureus
    • some streptococcus pneumonia
    • -: some Escherichia coli
    • some Klebsiella pneumoniae
    • some Proteus mirabilis
  35. 2nd gen cephalosporins microbial spectrum.
    gram + bacteria:
    gram - bacteria:
    Anaerobic bacteria:
    • +: activity similar to first generation
    • exceptions: cefoxitin & cefotetan have little activity
    • -: Escherichia coli
    • klebsiella pneumoniae
    • proteus mirabilis
    • haemophilus influ
    • Neisseria sp
    • anaerobic: cefoxitin & cefotetan have moderate anaerobic activity
  36. 3rd gen cephalosporin microbial spectrum.
    gram + bacteria:
    gram - bacteria:
    spirochetes:
    • +: Streptoococcus pyogenes
    • Viridans streptococci
    • many streptococcus pneumonia
    • modest activity against staphylococcus aureus
    • -: Escherichia coli
    • Klebsiella pneumoniae
    • Proteus sp
    • Haemophilus influ
    • Neisseria sp
    • some Enterobacteriaceae
    • Spirochetes: Borrelia burgdorferi
  37. Cefdinir dose and indication:
    pneumonia, community-acquired [300 mg PO q12hx10 days]
  38. Cephalexin dose and indication:
    infections, bacterial [1000-4000 mg/day PO divq6-12h]
  39. Most third generation cephalosporins do not have good activity against:
    The side chain of ceftazidime was modified to:
    • against P. aeruginosa. 
    • to increase its antipseudomonal activity. 
    • This modification makes it less active against S. aureus.
    • bottom line: when you modify one, you can be taking away from another. there is no perfect drug
  40. 4th gen cephalosporin, Cefepime, has very limited :
    Anaerobic activity
  41. Ceftaroline (Teflaro), a new IV cephalosporin for:
    it called to be what gen?
    wha should this drug be used for?
    • MRSA
    • "5th gen" cephalosporin but it doesn't have the extended gram - coverage that you might expect from a higher-gen cephalosporin
    • for drug-resistant infections
  42. what are the Carbapenems?
    • “The big guns”
    • Usually used for very severe infections or resistant organisms
  43. what kind of spectrum of activity do they have?
    broad
  44. what are the Cabapenems drugs?
    • Imipenem/cilastatin (Primaxin)
    • Meropenem (Merrem)
    • Ertapenem (Invanz)
    • Doripenem (Doribax)
  45. kinetics of carbapenems:
    • Administered parenterally
    • Excreted renally
    • Imipenim is hydrolyzed by an enzyme in the renal tubules.  Cilastatin is added to      prevent the metabolism of imipenim in        the kidney.
    • Renal impairment requires dosage adjustments (amount & frequency)
    • Ertapenem (Invanz)is administered once daily – on test!!!!
  46. SE of carbapenems:
    • N/V/D
    • Rash
    • Drug fever
    • Neurotoxicity; seizures   (may be on test)
  47. Doribax (Doripenem) 4th gen. Used for:
    • for complicated urinary tract, kidney, andintra-abdominal infections...but save it for resistant cases.      
    • Carbapenems are broad-spectrum IV antibiotics...coveringmany gram-positive and gram-negative organisms and anaerobes. Keep in mind none of these agents work for MRSA.
  48. Aztreonam (Azactam) kills:
    • Kills aerobic gram-negative bacteria
    • monobactam
  49. Glycopeptide drugs:
    Vancomycin
  50. Vancomycin is active against:
    • Gram + bacteria
    • A very large molecule which precludes it from passing through porins

    do NOT miss this on the test
  51. MOA of glycopeptides:
    • inhibits peptidoglycan synthesis
    • Glycopeptides inhibit cell wall synthesis by attaching to the end of the peptidoglycan precursor.
    • Due to the bulkiness of the vancomycin molecule, the enzyme that would incorporate the precursors into the growing peptidoglycan cannot access the precursor subunits.
    • Binding of the glycopeptide antibiotic to the end stops peptidoglycan synthesis. 
    • Cell wall synthesis is needed by the bacteria.
  52. how does resistance occur?
    • A change to the end of the amino acid precursor could mean that the glycopeptide antibiotic can no longer bind.*
    • Bacteria can produce excess cell wall
    • “Slimy way”- Staphylococcus epidermis can produce a film that blocks antibiotic penetration
  53. kinetics of glycopeptides:
    • Glycopeptides are very poorly absorbed from the GI tract; therefore oral administration is very effective for GI infections.
    • BUT, if infection is outside the GI tract, drug must be given IV
    • Trough levels are monitored with vancomycin.·        
    • THIS IS A DRUG THAT NEEDS MONITORING
    • Vancomycin half-life is 6 hours (don’t need to know)
    • Renal excretion.  Dose must be adjusted in renal impairment
  54. SE of glycopeptides:
    • Red Man Syndrome (usually assoc with rapid infusion) ON TEST!!
    • Fever
    • Nausea
    • Chills
    • Rash
    • Neutropenia (rare)
    • Flushing
    • Hearing loss, especially if given with an aminoglycoside
    • Nephrotoxicity

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