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240 Cards in this Set
- Front
- Back
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Name the antibiotics groups that are Cell Wall Synthesis Inhibitors.
Chapter 37: Principles of Antimicrobial Chemotherapy |
Beta-lactam antibiotics: carbapenems, cephalosporins, monobactams, and penicillins.
Others: bacitracin, fosfomycin, and vancomycin |
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Name the antibiotic groups that are Protein Synthesis Inhibitors.
Chapter 37: Principles of Antimicrobial Chemotherapy |
Aminoglycosides
Chloramphenicol Clindamycin Macrolides Mupirocin Streptogramins Tetracyclines |
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Name the antibiotic groups that are Folate Synthesis Inhibitors.
Chapter 37: Principles of Antimicrobial Chemotherapy |
Sulfonamides
Trimethoprim |
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Name the class of antibiotic that is a DNA Gyrase Inhibitor
Chapter 37: Principles of Antimicrobial Chemotherapy |
Fluoroquinolones
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Name the type of antibiotics that are RNA Polymerase Inhibitors.
Chapter 37: Principles of Antimicrobial Chemotherapy |
Rifampin
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Name the type of Antibiotics that are Cell Membrane Inhibitors.
Chapter 37: Principles of Antimicrobial Chemotherapy |
Amphotericin
Ketoconazole Polymyxin |
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An antibiotic that typically has more rapid effect and less likely to induce resistance is said to be....
Chapter 37: Principles of Antimicrobial Chemotherapy |
Bactericidal
(these tend to target cell wall or activated autolytic enzymes like penicillins) |
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An antibiotic that relies heavily on competent immune response is said to be......
Chapter 37: Principles of Antimicrobial Chemotherapy |
Bacteriostatic
(these tend to target metabolic pathways like the sulfonamides do) |
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Fill in the blank with either bacteriostatic or bactericidal.
Reversible inhibitors of protein synthesis are often __________ whereas, irreversible inhibitors are usually ________________. Chapter 37: Principles of Antimicrobial Chemotherapy |
bacteriostatic (tetracyclines)
bactericidal (streptomycin) |
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What is the term to describe that concentration of a drug that is required to inhibit growth of the pathogen?
Chapter 37: Principles of Antimicrobial Chemotherapy |
the MIC (minimal inhibitory concentration)
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What is the term used to ID the concentration that is required to kill the pathogen?
Chapter 37: Principles of Antimicrobial Chemotherapy |
MBC (minimal bactericidal concentration)
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What is the term that reflects the time required for the bacteria to return to log growth following drug withdrawal?
Chapter 37: Principles of Antimicrobial Chemotherapy |
PAE (Post-antibiotic effect)
Persistent suppression of bacterial growth after a limited exposure to a drug. The higher the PAE, the less number of doses needed. |
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Name two drugs that have long PAE's.
Chapter 37: Principles of Antimicrobial Chemotherapy |
Aminoglycosides (tobramycin)
Fluoroquinolones (ciprofloxacin) |
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List the three proposed mechanisms for PAE (Post-antibiotic effect)
Chapter 37: Principles of Antimicrobial Chemotherapy |
1) Recovery from non-lethal cell damage.
2) Persistence of drug at the site of action. 3) The need to synthesize new enzymes before new growth can occur. |
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Why is the PAE in vivo longer than in vitro?
Chapter 37: Principles of Antimicrobial Chemotherapy |
The PAE in vivo is longer than in vitro because of PALE
(post-antibiotic leukocyte enhancement) and due to the exposure of bacteria to subinhibitory drug concentrations. |
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What do Aminoglycosides and once-daily quinolones have in common?
Chapter 37: Principles of Antimicrobial Chemotherapy |
They both have concentration-dependent PAE.
(for instance, aminoglycosides remain effective for some time after serum levels of the drug drop below the MIC of a given organism.) PAE=Post-Antibiotic Effect MIC=Minimal inhibitory concentration |
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T/F Typically, the pharmacokinetics are similar whether antimicrobials are given orally or parentally.
Chapter 37: Principles of Antimicrobial Chemotherapy |
TRUE
ORAL: less costly and fewer side effects IV: Critically ill patients, bacterial meningitis or endocarditis Nausea, vomiting, gastrectomy |
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EAR INFECTION? Give....
Chapter 37: Principles of Antimicrobial Chemotherapy |
Amoxicillin
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In what circumstances would antimicrobial pharmacokinetics be altered?
Chapter 37: Principles of Antimicrobial Chemotherapy |
-Renal or hepatic insufficiency
-Burns, cystic fibrosis -Elderly, neonates, pregnancy |
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What happens in the treatment of enterococcal endocarditis?
Chapter 37: Principles of Antimicrobial Chemotherapy |
Synergy!!
Penicillins and vancomycin are BACTERIOSTATIC in monotherapy for this infection, but when combined with an aminoglycoside, BACTERICIDAL activity results. |
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List the three mechanisms of antimicrobial synergism.
Chapter 37: Principles of Antimicrobial Chemotherapy |
1) Blockade of sequential steps in a metabolic sequence.
2) Inhibition of enzymatic inactivation. 3) Enhancement of Antimicrobial Agent uptake Examples of 1) TMP-SMX block sequential steps in folate pathway. 2) Inhibition of B-lactamase 3) Penicillins increase bacterial uptake of aminoglycosides |
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In surgical prophylaxis, what determines if and when and what type of antibiotics should be used?
What is the drug of choice for most procedures? Chapter 37: Principles of Antimicrobial Chemotherapy |
-The Antibiotic should be specific for common surgical wound pathogens
(not a broad spectrum). -They must have proven efficacy in clinical trials. -Concentration > MIC at the time of incision. -Single dose - DOC for most procedures is Cefazolin. |
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What is Cefazolin?
Chapter 37: Principles of Antimicrobial Chemotherapy |
It is a cephalosporin (a B-lactam) Cell Wall Synthesis Inhibitor.
It is also the drug of choice for most surgical procedures. |
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What is the prophylactic drug of choice in suspected exposure to Anthrax?
Chapter 37: Principles of Antimicrobial Chemotherapy |
Ciprofloxacin (long PAE)
or Doxycycline |
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What is the prophylactic drug of choice when there has
been close contact with Cholera? Chapter 37: Principles of Antimicrobial Chemotherapy |
Tetracycline
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What is the prophylactic drug of choice when dental procedures are done in at-risk patients (like prosthetic heart valves or cardiac malformations)?
Chapter 37: Principles of Antimicrobial Chemotherapy |
amoxicillin
or clindamycin |
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What is the prophylactic drug of choice for HIV when there is blood exposure by needle stick?
Chapter 37: Principles of Antimicrobial Chemotherapy |
zidovudine + lamivudine
(+/- indinvir or nelfinivir) |
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What is the prophylactic drug of choice of Otitis Media when there are recurrent infections?
Chapter 37: Principles of Antimicrobial Chemotherapy |
Amoxicillin
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What are B-lactamases and what do they do?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
They are bacterial enzymes which hydrolyze the B-lactam ring and inactivate the antibiotic.
In other words, they degrade the penicillins. |
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List the B-Lactam Antibiotics.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Penicillins
Cephalosporins Monobactams Carbapenems B-lactamase inhibitors |
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What are the narrow spectrum antiobiotics?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
penicillin G
penicillin V (these were originally isolated from Penicillium) |
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What are the Penicillinase resistant penicillins?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
dicloxacillin
nafcillin |
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What are the extended spectrum penicillins?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
amoxicillin
ampicillin piperacillin ticarcillin |
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What is the collective term for the bacterial enzymes that are responsible for the assembly, maintenance and regulation of the peptidoglycan portion of the cell wall?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Penicillin-binding proteins (PBP)
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What do the B-lactam antibiotics do?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
They covalently bind to PBPs.
PBP = penicillin-binding proteins |
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What does inhibition of PBP-1 and PBP-2 do?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
inhibition of PBP-1 prevents cross-linking of peptidoglycan
inhibition of PBP-2 results in loss of rod shape. PBP = penicillin binding proteins |
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What is peptidoglycan?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Linear strands of two alternating amino sugars (N-acetylglucosamine and N-acetylmuramic acid) which are crosslinked by a peptide chain.
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What catalyzes the linkage of the peptide chains in peptidoglycan?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
a transpeptidase.
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Where does pencillin bind?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It binds irreversibly at the active site of the transpeptidase.
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Penicillin binds irreversibly at the active site of the transpeptidase. In doing this, what is it mimicking?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Penicillin mimics the D-alanyl-D-alanine residues that would normally bind to the active site of the transpeptidase.
Remember, the transpeptidase catalyzes the crosslinking of the two alternating amino sugars that make up peptidoglycan. |
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Name the Acid-stable (oral) penicillins.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
amoxicillin
dicloxacillin nafcillin pencillin V (penicillin G in large doses) |
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Name the Acid-labile (parenteral) pencillins.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
piperacillin
ticarcillin |
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Penicillin G is destroyed by gastric fluid at pH 2.
Explain how this plays out in the elderly? Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
The decrease in gastric acid production with age
accounts for the better absorption in the elderly. |
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The penicillins are widely distributed except for a few places. Where?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Brain
Prostatic secretions intraocular secretion (They do enter the CNS when the meninges are inflammed) |
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What is the half life of the penicillins?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
t 1/2 is 30-90 min
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How are the penicillins rapidly eliminated?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Glomerular Filtration and
Renal Tubular Secretion |
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Penicillins are rapidly eliminated by glomerular filtration and renal tubular secretion. There are two that are excreted also in the bile. What are they?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Ampicillin and nafcillin
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What drug competes with the penicillins for the organic acid transporter in the proximal tubule?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Probenecid
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Why is Probenecid used?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It is a treatment for gout, but it is also used to prolong the half-life of penicillin G because probenecid competes with the penicillins for the transporter in the proximal tubules.
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Name two penicillins that are long-acting IM preparations.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Procaine penicillin G
Benzathine penicillin G (great to give when pts can't take orally or in cases where compliance is an issue) |
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The narrow spectrum penicillin, Penicillin G, is used to treat......
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
-Syphilis (Treponema pallidum)
-Menigitis (Meningococci) -Pneumonia (Pneumococci) (gram + cocci) |
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When using Penicillin G, until is it certain that the infecting isolate is penicillin-sensitive, what is indicated?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
A third generation cephalosporin
or vancomycin |
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What is Penicillin V used for?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Pharyngitis (Streptococcus pyogenes)
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What are the penicillinase-resistant penicillins and how are they produced?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Dicloxacillin
Nafcillin They are semi-synthetic and are produced from 6-aminopenicillanic acid. |
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What are Dicloxacillin and Nafcillin used for?
What type of penicillins are they? Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
They are used to treat serious penicillinase-producing staphylococci in
-Osteomyelitis -Endocarditis -Skin/soft tissue infections Dicloxacillin (oral) Nafcillin (parenteral) "Naf for Staff" |
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Staph infections that are resistant to the penicillinase-resistant penicillins are termed methicillin resistant Staphylococcus aureus (MRSA) What is the DOC?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Vancomycin
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Many staph infections are problematic due to the fact that they have a lot of _____________.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
penicillinase.
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Dicloxacillin and Nafcillin are penicillinase-resistant penicillins. What type of bacteria are they NOT effective against?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Gram (-) bacteria
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What are the aminopenicillins and what type of penicillins are they?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Amoxicillin and Ampicillin are Extended Spectrum Penicillins
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What are the aminopenicillins "extended" to include?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Gram (-) microorganisms like
H. influenzea E. coli Proteus mirabilis |
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What is Amoxicillin used to treat?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Otitis
URT (S. pneumoniae and H. influenzae) (Amoxicillin is one of the Aminopenicillins which are Extended Spectrum Penicillins) |
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What is used to treat Meningitis due to L. monocytogenes in immunocompromised individuals?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Ampicillin
(It is NOT used when meningitis is caused by S. pneumoniae which is often the case in children) |
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What is the emperic treatment of suspected bacterial meningitis?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Ampicillin + vancomycin + 3rd generation cephalosporing
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Name the anti-pseudomonal Extended Spectrum Penicillin.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Piperacillin
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What are the Antipseudomonals used to treat?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Gram (-) organisms, primarily P. aeruginosa
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What is Piperacillin used to treat?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
nosocomial pneumonia suspected to be caused by P. aeruginosa
Piperacillin is an Antipseudomonal, Extended Spectrum penicillin |
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Explain the Hypersensitivity Response to penicillin.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
The degradation products of penicillin combine with protein to form antigenic comopounds.
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The hypersensitivity response to penicillin is mediated by_________
What are the symptoms of this reaction? Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
IgE mediated response
-Rash -Nephritis -Serum sickness -Anaphylactic shock |
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What drugs are used against penicillin-sensitive Streptococcus pneumoniae?
(there are three) Lecture Review Questions |
amoxicillin (kids)
azithromycin ceftriaxone |
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What drug is used against penicillin-resistant Streptococcus pneumoniae?
Lecture Review Questions |
levo-moxifloxacin
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What drug is used for Acute Pharyngitis?
Lecture Review Questions |
benzathine penicillin G
IM, it's a quick, easy fix |
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What drug is used for Scarlet Fever (Streptococcus)?
Lecture Review Questions |
benzathine penicillin G
IM, it's one dose. done! |
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Treatment for Acute Otitis Media?
Lecture Review Questions |
amoxicillin
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Treatment for Helicobacter pylori infection?
Lecture Review Questions |
amoxicillin
clarithromycin |
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Treatment for Staphylococcal Impetigo?
Lecture Review Questions |
dicloxacillin
cephalexin mupirocin (topical) |
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Treatment for Streptococcal Impetigo?
Lecture Review Questions |
amoxicillin
mupirocin (topical) |
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Treatment for Klebsiella pneumoniae infection?
Lecture Review Questions |
imipenem / meropenem
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Treatment for Meningococcemia (N. meningitidis)?
Lecture Review Questions |
cefotaxime
ceftriaxone (3rd generation cephalosporins that enter the CNS) |
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Treatment of Pseudomonas infections in the Heart?
in the lungs? in the CNS? Lecture Review Questions |
Heart: tobramycin
Lung: piperacillin (key anti-pseudomonal agent) CNS: (cefepime/ceftazidime) + gentamicin |
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Which of the following is indicated for treatment of bacterial meningitis (H. influenzae) in a 2 year old boy?
-cefotaxime -cefoxitin -cefprozil -penicillin G -vancomycin Lecture Review Questions |
Cefotaxime
Third generation cephalosporins cross the CNS and are effective against gram negative organisms. |
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An adult female presents with a urinary tract infection caused by an aerobic gram-negative bacillus. she has previously had a hypersensitivity reaction to penicillin G. Which of these agents is indicated?
-cefazolin -clavulanic acid -imipenem -aztreonam -amoxicillin Lecture Review Questions |
aztreonam
it is generally safe in those who are allergic to penicillins and cephalosporins. It's a monobactam effective against many aerobic Gram (-). |
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Which of the following parenterally administered agents would be most effective against B-lactamase producing strains of H. influenzae and N. gonorrhoeae?
-Amoxicillin -Ceftriaxone -Piperacillin -Penicillin G Lecture Review Questions |
Ceftriaxone
It's a 3rd generation Cephalosporin. These have a wider range of activity against Gram (-). Most enter CNS. |
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Which of the following agents is the most active against Pseudomonas aeruginosa?
-Ampicillin -Penicillin G -Penicillin V -Nafcillin -Piperacillin Lecture Review Questions |
Piperacillin
It is an extended spectrum, antipseudomonal drug. |
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An adult female is admitted to the hospital with endocarditis caused by a pencillinases-producing Staphylococcus aureus infection and requires parenteral therapy. Which of the following agents is indicated?
-Ampicillin -Amoxicillin -Nafcillin -Penicillin G Lecture Review Questions |
Nafcillin
It is penicillinase-resistant and typically given parenterally. |
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Cephalosporins are more stable than penicillins. Why?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Because they are highly resistant to penicillinase.
They are also less likely to cause hypersensitivity reactions |
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What are 1st generation cephalosporins primarily active against?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
most gram (+) cocci
(not MRSA or enterococci) ans some gram (-) organisms. |
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T/F Cephalosporins are given orally and are readily absorbed from the gut; food has minimal effect on its bioavailability.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
True
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How are Cephalosporins cleared?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Renal excretion except for
ceftriaxone which is excreted in bile. |
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List the 1st generation Cephalosporins.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Cephalexin (oral)
Cefazolin (parenteral) |
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Name what Cephalexin is used for.
What generation Cephalosporin is it? How is it given? Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
-Skin and soft tissue infections
-Streptococci -Orally |
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What is Cefazolin used for?
What generation Cephalosporin is it? How is it given? Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
-more serious streptococci
-surgical prophylaxis against staphylococci and gram (-) enteric bacilli -parenterally |
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Which of the first generation Cephalosporins is preferred to its longer half-life?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Cefazolin
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Which generations of Cephalosporins do NOT enter the CNS?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
1st
2nd some 3rd |
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Name the 2nd Generation Cephalosporins.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Cefprozil (oral)
Cefuroxime sodium Cefoletan Cefoxitin |
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Name the 2nd Generation Cephalosporins and whey they are used for.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
-Cefprozil (oral) for Otitis that is caused by amoxicillin resistant H. influenzae
-Cefuroxime sodium - emperic therapy for community-acquired pneumonia. (only 2nd gen to enter CNS) -Cefoletan - Intra-abdominal, gynecologic and biliary tract infections -Cefoxitin - surgical prophylaxis |
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Which drug is the only 2nd generation Cephalosporin that enters the CNS?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Cefuroxime sodium
(it's used as emperic therapy for community-acquired pneumonia) |
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List the 3rd generation Cephalosporins.
What organisms are they used against? Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
-Cefotaxime
-Ceftriaxone Used against a wider range of activity against Gram (-) organisms that include: Enterobacteriacae H. influenzae M. catarrhalis |
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Cefotaxime and Ceftriaxone are used to treat.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Gonorrhea
Urinary tract and intra-abdominal infections otitis media meningitis pneumonia Lyme disease These are 3rd generation Cephalosporins - most enter the CNS. |
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Name the 4th generation Cephalosporin and what it targets.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Cefepime
-Targets gram (-) bacteria Particulalry nosocomial pathogens like Citrobacter freundii Enterobacter cloacae which are generally resistant to other cephalosporins. |
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What is special about Cefepime?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It is very resistant to BLM.
It enters the CNS It's the only 4th generation Cephalosporin BLM= B-lactamases |
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Cephalosporins are NOT effective against.........
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
LAME organisms
L-isteria monocytogenes -Atypicals like Chlamydia and Mycoplasma -MRSA -Enterococci |
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Cephalosporins may have cross-sensitivity with penicillins. Explain what happens if there is a mild vs severe reaction to penicillin.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
If MILD reaction to penicillin then cephalosporins are usually tolerable.
If SEVERE reaction to penicillin then cephalosporins are contraindicated. |
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Bacterial resistance can occur through four mechanisms.
List them. Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
1. Inactivation of the drug by B-lactamase enzymes.
2. Reduced affinity of penicillin-binding proteins for the drug. 3. Efflux pumps 4. Decreased entry of the drug into bacteria through the outer membrane porins. |
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How do we treat to overcome the B-lactamase enzymes?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
We combine penicillins with B-lactamase inhibitors.
Amoxicillin + clavulanate Ampicillin + sulbactam Piperacillin + tazobactam |
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Decreased entry of the durg into bacteria through the outer membrane porins has to do with Gram (-) cell membrane structure. Explain.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
In gram (-) bacteria, the PBP are very near the cell surface thus more easily accessible. But the outer membrane is oan impenetrable barrier to some antibiotics. However, hydrophilic antibiotics diffuse through aqueous channels, porins.
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How is P. aeruginosa intrinsically resistant to antibiotics?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
They have a relatively low number of aqueous channels, porins, that would let the hydrophilic antibiotics into the cell.
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What are the three B-lactamase inhibitors?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Clavulanate
Sulbactam Tazobactam |
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How do B-lactamase inhibitors work?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
They irreversibly bind to B-lactamases that many bacteria produce.
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What are B-lactamase inhibitors inactive against?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Inactive against type I chromosomal BLMs that are induced in
Enterobacter Acinetobacter Citrobacter by 2nd & 3rd gen cephalosporins. |
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Name the Monobactam and what it is effective against.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Aztreonam (It's a monocyclic B-lactam)
effective against AEROBIC Gram (-) bacteria: Enterobacter Citrobacter Klebsiella Proteus P. aeruginosa |
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What's so great about Aztreonam?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It's resistant to many of the B-lactamases produced by gram (-) bacterial.
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What's not so great about Aztreonam?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Gram (+) and anaerobic bacteria are resistant to it.
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How do patients that are allergic to penicillins and cephalosporins generally react to Aztreonam?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
They are generally NOT allergic to it.
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Name the Carbapenems and what they are active against.
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Imipenem
Meropenem Against lots of Gram (+) and Gram (-) including many AEROBIC and ANAEROBIC Gram (-) bacilli. |
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What kind of infections are Imipenem and Meropenem good for?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Systemic infections, esp mixed infections that are caused by aerobic and anaerobic enteric bacilli.
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What is Impenem inactivated by? How do we circumvent this problem?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Renal Dehydropeptidase
We give the enzyme inhibitor, cilastin, in conjuction with the Imipenem. |
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What drug inhibits the renal excretion of Carbapenems?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Probenecid
It's a drug used to treat gout. We also use it with penicillins to increase the half-life of the penicillins because they compete for the acid transporter in the proximal tubule. |
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There is cross-sensitivity of Carbapenems with penicillins, cephalosporins and other B-lactams. What do we do in allergic patients?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Avoid!!
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What is Vancomycin?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It's another key bacterial cell wall synthesis inhibitor, not a B-lactam antibiotic.
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What is Vancomycin used against?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Several Gram (+) cocci and bacilli
Esp Serious infections caused by penicillin-resistant organisms like -MRSA -enterococci |
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Where is vancomycin poorly absorbed?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
in the gut
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What is bacitracin?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It is one of the other key bacterial cell wall synthesis inhibitors that is not a (b-lactam antibiotic)
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What is Bacitracin used against?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It's a topical treatment of minor skin and ocular infections.
Esp against Gram POSITIVE staphylococci and streptococci |
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What is Fosfomycin?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It is one of the other key bacterial cell wall synthesis inhibitors that is not a (b-lactam antibiotic)
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What is Fosfomycin used for?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
To treat uncomplicated Urinary Tract infections.
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How does Fosfomycin work?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It irreversibly inhibits enopyruvyl transferase in the initial stages of cell wall peptidoglycan synthesis.
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How is Fosfomycin dosed?
Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
It is a single oral dose which is excreted unchanged in the urine and feces.
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The Inhibitors of Bacterial Protein Synthesis selectively disrupt bacterial protein synthesis by exploiting the differences in what?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Differences in bacterial Ribosome Structure and Function.
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Where do tetracyclines bind? What do they prevent?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Tetracyclines bind to the 30S bacterial ribosome and prevent access of aminoacyl-tRNA to the A site.
|
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How do Aminoglycosides work?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
They block initiation of protein synthesis by fixing the 30S/50S complex at the start codon.
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When the aminoglycosides fix the 30S/50S complex at the start codon, what does this cause?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
casues a misreading of mRNA leading t0
-premature termination of translation -incorporation of an incorrect amino acid -abnormal protein is then made |
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What is peptidyl transferase and what does it do?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
It an enzyme that catalyzes the formation of a peptide bond between the new a.a. and the nascent peptide
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What agents act to stop peptidyl transferase? How do they do it?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Macrolides
Chloramphenicol Dalfopristin They bind the 50S and prevent appropriate enzyme-0substrate interaction. |
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What drug groups affect the 30S Ribosomal Subunit?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Aminoglycosides
Tetracyclines |
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Name the Aminoglycosides.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Amikacin
Gentamicin Neomycin Streptomycin Tobramycin |
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Name the Tetracyclines
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Tetracycline
Doxycycline Minocyclin |
|
|
What are the adverse effects of the Aminoglycosides?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Nephrotoxicity - accumulation in P.T. what results in acute necrosis.
Ototoxicity - Accumulation in the labyrinth and hair cells of the cochlea. |
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Aminoglycosides are highly basic and become protonated and ionized in body fluids. What does this mean practically?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
-They do not readily enter host cells or cross the BBB.
-They are inactivated by acetylase, adenylase and phosphorylase. |
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|
T/F Aminoglycosides are rapidly bactericidal, concentration dependent, and blocked by low pH, anaerobiasis, and divalent cations.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
TRUE
|
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How are Aminoglycosides administered?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Parenterally for systemic infections
Topically for infections of the skin,mucous membranes and eyes. |
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|
Are Aminoglycosides metabolized?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
No, they are excreted by renal glomerular filtration.
|
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In the presence of renal impairment, what should be done with Aminoglycosides?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Reduce the dose
|
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|
What are aminoglycosides?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
amino sugars linked through glycosidic bonds
-poorly absorbed from the gut. |
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How do Aminoglycosides enter the cells?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
They diffuse through porin formed channels in the outer membrane but then enter into the periplasmic space.
Movement across the inner membrane requires an oxygen and energy dependent transport. |
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What type of micro-organisms do the aminoglycosides work against?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
AEROBIC Gram (-) bacilli
|
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Which aminoglycoside is used to treat multi-drug resistant TB, plague (Yersinia pestis) and tularemia (Francisella tularensis)?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Streptomycin
|
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What aminoglycoside is msot active against the Enterobacteriaceae species?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Gentamicin
|
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|
What aminoglycoside is most active against P. aeruginosa?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Tobramycin
|
|
|
What aminoglycoside is resistant to enzyme inactivation?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Amikacin
Used when infection is resistant to other aminoglycosides. |
|
|
Which aminoglycoside is the MOST NEphrotoxic?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Neomycin
Therefore it's use is limited to topical treatments. |
|
|
What is special about the tetracycline, Minocycline?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
It is Anti-bacterial, anti-inflammatory and gets into the brain.
|
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|
How do tetracyclines affect antibacterial activit?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
They bind to the 30S bacterial ribosome and prevent access of aminoacyl-tRNA to the A site.
|
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T/F If a person is immunocompromised then you don't want to use a Bacteriostatic drug.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
True
|
|
|
What are the adverse effects of tetracyclines?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Discoloration of teeth
Photosensitivity |
|
|
What is the mechanism that causes the adverse effect of photosensitivity with tetracyclines?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
The drug accumulates under the skin and absorbs UV radiation. Emission of this energy damages skin and leads to sunburn-like condition.
|
|
|
How are tetracyclines gotten rid of from the body?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
They are excreted in urine and feces.
|
|
|
Which tetracycline is NOT dependent upon renal elimination?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Doxycycline
|
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|
Which tetracycline reaches the CNS and penetrates the skin more efficiently?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Minocycline
|
|
|
Discuss the oral bioavailability of tetracyclines.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Oral Bioavailability is > 70%
They bind divalent and trivalant cations (Ca, Al and Fe) Bioavailibility is reduced by certain foods Do not take with antacids or iron supplements. |
|
|
Tetracylcines are the drugs of choice for what diseases?
There are 5. Chapter 39: Inhibitors of Bacterial Protein Synthesis |
1. Rocky Mt. Spotted fever (Rickettsia)
2. Lyme Disease 3. Acne Vulgaris 4. Genital infections caused by Chlamydia (Doxycyline) 5. Peptic ulcers caused by H. pylori |
|
|
What tetracycline is used for genital infections casued by Chlamydia?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
doxycyline
|
|
|
What drugs are used for peptic ulcers caused by H. pylori?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
tetracyclines
|
|
|
What drug is used for a Borrelia durgdorferi infection?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Doxycycline
|
|
|
What drug(s) is used for a Treponema pallidum infection?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Benzathine penicillin G
Doxycycline (alternate) |
|
|
What is the drug of choice for Rocky Mountain Spotted Fever (Rickettsia rickettsii)?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
doxycycline
|
|
|
That is the drug of choice for Lyme disease?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
doxycycline
|
|
|
The 30S ribosomal function is inhibited by what two drug groups?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Aminoglycosides
and Tetracyclines |
|
|
Aminoglycosides are active against what kind of bacteria?
Give one example. Chapter 39: Inhibitors of Bacterial Protein Synthesis |
AEROBIC gram (-) bacteria
example: P. aeruginosa |
|
|
T/F Tetracyclines are bacteriostatic and broad spectrum.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
True
|
|
|
T/F/ Aminoglycosides are poorly absorbed.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
True
|
|
|
What drugs affect the 50S Ribosomal Subunit?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Macrolides
Chloramphenicol Clindamycin Quinupristin-Dalfopristin Linezolid |
|
|
Name the Macrolides.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Azithromycin
Clarithromycin Erythromycin |
|
|
What is the mechanism of action of the macrolides?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Bind the 50S ribosomal subunit and prevent translocation of the nascent peptide from the A site to the P site.
This blockade inhibits biding of the next aminoacyl tRNA to the ribosome. |
|
|
How are macrolides given and how are they excreted?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Orally
Excreted in bile and urine |
|
|
The absorption and activity of erythromycin is reduced by......
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
gastric acid
|
|
|
Which two of the macrolides are more readily absorbed, have a longer helf life and acienve higher tissue concentraions?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Azythromycin
and clarithromycin |
|
|
Which two macrolides are less likely to cause GI distress?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Azithromycin
and clarithromycin |
|
|
Which macrolides inhibit CYP3A4?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Erythromycin
and clarithromycin This can result in toxicity of certain drugs that require this enzyme for elimination. |
|
|
What effect does Azithromycin have on the CYP3A4 enzyme?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
little effect at all.
|
|
|
Upper Respiratory Infections and pneumonia are are treated with?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Macrolides
Streptococci Pneumococci Chlamydiae H. influenzae (otitis media and sinusitis) M. pneumoniae L. pneumophila H. pylori |
|
|
Which bacterial infections are especially treated with Azithromycin?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Chlamydiae
H. influenzae (otitis media, sinusitis) M. pneumoniae L. pneumophila |
|
|
What bacteria is Clarithromycin the most active macrolide against?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
H. pylori
|
|
|
What do these drugs have in common?
-Chloramphenicol -Clindamycin -Quinupristin-Dalfopristin -Linezolid -Mupirocin Chapter 39: Inhibitors of Bacterial Protein Synthesis |
They are macrolides that affect the 50S ribosomal subunit.
|
|
|
Describe the mechanism of action of erythromycin.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Similar to erythromycin:
-Binds the 50S subunit of bacterial ribosomes and suppresses protein synthesis. -It's binding site is similar to macrolides and chloramphenicol. |
|
|
What is so important to remember about Clindamycin?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
1) It is NOT readily enter the CNS
2) So there is a high risk of GI superinfection Clostridium difficile growth is enhanced by the altered gut flora Watch for severe diarrhea -can be fatal |
|
|
How is Clindamycin excreted from the body?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Excreted in bile and urine
|
|
|
What is the antibacterial activity of of clindamycin?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
1) Penicillin-resistant Streptococci
2) Anaerobic bacteria Bacteroides fragilis Clostridium perfringens |
|
|
If a pt has been on clindamycin and they have severe diarrhea, what should be done?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Discontinue use of clindamycin
Treat with metronidazole or vancomycin |
|
|
What is the mechanism of action of Chloramphenicol?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Binds the 50S subunit at the peptidyltransferase site and thereby inhibits transpeptidation.
|
|
|
T/F Chloramphenicol is considered a broad spectrum antiobiotic.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
TRUE
Used to treat meningitis caused by pneumoccoci, meningococci and H. influenzae. |
|
|
How is chloramphenicol metabolized?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
it's metabolized by glucuronate conjugation and excreted in the urine.
|
|
|
Why must chloramphenicol be reduced in neonates?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Neonates are relatively deficient in glucuronosyl-transferase. So drug levels of chloramphenicol must be reduced in order to prevent severe toxicity.
|
|
|
Describe Chloramphenicol.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
It is an antibiotic that affects the 50S ribosomal subunit.
It is highly lipophilic. It readily enters the CNS |
|
|
Name the newer class of antibiotics called streptogramins.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Quinupristin
Dalfopristin |
|
|
How are the streptogramins administered?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
I.V.
It has wide distribution (NOT CNS) |
|
|
How does Quinupristin work?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Inhibits the synthesis of tFNA.
It's mechanism of action is similar to macrolides, thus prevents the addition of new a.a. to the nascent peptide chain. |
|
|
How does Dalfopristin work?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Inhibits peptidyl transferase
It synergystically enhances binding of quinupristin Blocks the formation of the peptide bond. |
|
|
What is the combination, Quinupristin-Dalfopristin used to treat?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Used to treat
vancomycin-resistant organisms |
|
|
Does Quinupristin-Dalfopristin enter the CNS?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
No
it has a wide distribution, just does not include the CNS |
|
|
Name a drug from the new class called oxazolidinediones.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Linezolid
|
|
|
How is linezolid administered?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
I.V. or oral
Oral bioavailability is 100% About 30% of the drug is excreted unchanged in the urine |
|
|
How does Linezolid work?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Binds the 23S ribosomal RNA of the 50S subunit. This prevents the formation of a functional 70S initiation complx.
Because of this unique mechanism of action, Cross-resistance is unlikely. |
|
|
What kind of organisms is Linezolid active against?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Many AEROBIC gram (+) positive
Esp -Vancomycin-resistant E. faecium -MRSA |
|
|
Describe the structure of Mupirocin.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
It's structure is unrelated to other antibiotics.
It contains a side chain that is similar to isoleucine. So it competes for bacterial ISOLEUCINE tRNA synthetase (the enzyme which catalyzes the formation of isoleucyl tRNA) Does not exhibit cross-resistance |
|
|
What is Mupirocin active against?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
most Staphylococci
|
|
|
What is the first effective topical therapy for impetigo (either streptococci or staphylococci)?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Mupirocin
|
|
|
Describe the three possible ways bacterial resistance to protein synthesis inhibitors develops.
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
1. Inactivation of the drug by bacterial enzymes
2. Decreased drug binding 3. Decrased drug accumulation |
|
|
How does bacteria develop resistance to protein synthesis inhibitors by decreasing drug binding?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
two ways:
-Decreased binding of aminoglycosides to 30S ribosomal subunit -Decreased binding of macrolides to 50S ribosomal subunit. |
|
|
How does bacteria develop resistance to protein synthesis inhibitors by decreasing drug accumulation?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
two ways:
-active removal of the drug -decreased uptake of the drug |
|
|
What is the drug of choice for Bordetella pertussis?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
azithromycin
|
|
|
What is the drug of choice for Acne vulgaris?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
tretinoin (vit A)
erythromycin clindamycin |
|
|
How does bacteria develop resistance to protein synthesis inhibitors by decreasing drug binding?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
two ways:
-Decreased binding of aminoglycosides to 30S ribosomal subunit -Decreased binding of macrolides to 50S ribosomal subunit. |
|
|
What is the drug of choice for Bordetella pertussis?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Azithromycin
|
|
|
What are the drugs of choice for Acne vulgaris?
Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Tretinoin (vit A)
Erythromycin Clindamycin |
|
|
An 8 y.o. pt presents with pharyngitis caused by Chlamydia pneumoniae. Previously this child had an adverse reaction to amoxicillin. Which of the following is the most appropriate oral therapy?
-Azithromycin -Cephalezin -Piperacillin -Penicillin G -Vancomycin Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Azithromycin
a macrolide, very effective against otitis and upper respiratory infections. Vancomycin could kinda, but it's not readily absorbed when administered orally, and so it's reserved for more serious infections. |
|
|
Which of the following agents acts at the 50S ribosomal subunit to inhibit translocation of peptidyl-mRNA from the acceptor site to the donor site?
-Azithromycin -Doxycycline -Gentamycin -Mupirocin -Tetracycline Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Azithromycin (a macrolide, other macrolides include clarithromycin and erythromycin.)
|
|
|
Which of the following requires a 7-day course of treatment in order to be effective against uncomplicated gonorrhea?
-Azithromycin -Cetfriaxone -Ciprofloxacin -Doxycycline -Fosfomycin Chapter 39: Inhibitors of Bacterial Protein Synthesis |
Doxycycline
must be given for 7 days non-compliance is an issue |
|
|
H. Influenzae, M. catarrhalis and N. gonorrhoeae are all Beta-lactamase producers. Which of the following is effective against ALL of these organisms?
-Amoxicillin -Ceftriaxone -Clindamycin -TMP-SMX -Tecarcillin Chapter 38: Inhibitors of Bacterial Cell Wall Synthesis |
Ceftriaxone (IM) is the drug of choice.
Cefepime (4th generation) is also effective. |
|
|
Name the antifolate drugs.
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
-Sulfamethoxazole (SMX)
-Trimethoprim (TMP) |
|
|
Name the Fluoroquinolones.
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
-Ciprofloxacin
-Levofloxacin |
|
|
Folate is necessary for DNA synthesis.
Humans obtain preformed folate in the diet. How do bacteria obtain folate? Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Folate synthesis in bacteria is initiated with the fusion of pteridine and p-aminobenzoic acid (PABA) to form dihydrofolate.
|
|
|
How do Sulfamethoxazole and Trimethoprim work?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Sulfamethoxazole and Trimethoprim inhibit sequential steps of DNA synthesis.
|
|
|
What is the difference between how Trimethoprim binds to bacterial vs mammalian folate reductase?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
TMP binds bacterial folate reductase with 100k fold greater affinity compared to the mammalian enzyme.
|
|
|
Name the sulfonamides.
(there are three) Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
-sulfamethoxazole
-silver sulfadiazine -sulfacetamide |
|
|
At what step in folate synthesis does Sulfamethoxazole work?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
it works at the Dihydropteroate synthase step
|
|
|
What is sulfamethoxazole used for and by what mechanism?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Rapidly absorbed
Used primarily to treat urinary tract infections The drug is inactivated by N-acetylation - the insoluble acetylated meabolite can precipate in the renal tubules causeing crysatalluria. (sufficient hydration is mandatory) |
|
|
What is a topical sulfonamide used to treat ocular infections?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Sulfacetamide.
|
|
|
Name a sulfonamide that is used to prevent infection of burns.
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Silver Sulfadiazine
|
|
|
Name a sulfonamide that is used to primarily treat urinary tract infections.
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Sulfamethoxazole
|
|
|
What would you use for "pink eye" assuming it's a bacterial infection?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Sulfacetamide.
|
|
|
What drug is used to treat bacterial prostatitis and vaginitis?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Trimethoprim
|
|
|
What drug is a synthetic aminopyrimidine drug that is a weak base, so it is concentrated in tissue that are more acidic than plasma such as in prostate and vaginal fluids?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Trimethoprim
|
|
|
Trimethoprim-Sulfamethoxazole is used to treat what?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Primarily used to treat urinary tract and prostate infections from
-E. coli -K. pneumonia -Proteus species -Enterobacter species |
|
|
What is the drug of choice for pulmonary infections caused by
Pneumocycstic jiroveci (fungal); and Nocardia asteroides (typically in immunocompromised patients)? Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Trimethorprim-Sulfamethoxazole
(TMP-SMX) |
|
|
What cause of urinary tract infections is TMP-SMX NOT an active agent against?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Pseudomonas aeruginosa, which is often the cause of UTI in hospitalized patients.
|
|
|
What
List the Fluoroquinolones. Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
-Ciprofloxacin
-Levofloxacin -Moxifloxacin -Gatifloxacin -Gemifloxacin |
|
|
Which fluoroquinolone is very effective agaisnt gram (-) bacteria, but less-so against gram (+)?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Ciprofloxacin
|
|
|
Which fluoroquinolone has increased activity against pneumococci?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Moxifloxacin
|
|
|
T/F Fluoroquinoles are well absorbed and widely distributed. They are more concentreated in many tissues compared to plasma.
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
True
They are more concentrated in the lungs, kidneys, prostate, endometrium and ovaries. |
|
|
Fluoroquinolones are DNA gyrase inhibitors. Do they have a long PAE?
Chapter 40: Quinolones, Antifolate Drugs, and other Antimicrobial Agents |
Yes, they have a long post antibiotic effect.
They are bactericidal. They use concentration-dependent killing |
