Penicillin 2

Front 1

1. What characteristic sets aminopenicillins apart?
2. What does the characteristic help with?
3. What are the 2 e.g.?

Back 1

1. NH2 group on the side chain
2. Helps get through the porins of outer membrane of GM-, but weaker than natural penicillin against gram +
3. Amoxicillin, Ampicilin

Front 2

Aminopenicillin: ampicillin vs amoxicillin
1. Which is paraenteral?
2. Which is oral
3. What does this penicillin produce more often than other penicillins?

Back 2

1. Ampicillin
2. Both, but amoxicillin is better b/c it lasts longer in the body
3. A rash (nonallergenic) that resolves naturally, not a reason to discontinue treatment

Front 3

1. Of the oral Beta-penicillins, diarrhea is most frequently associated with which?

Back 3

1. Amoxicillin-clavulanate

Front 4

1. What 3 drugs are useful against pseudomonas?
2. What classes are they from?
3. Why were some discontinued?

Back 4

1. TCP - Ticarcillin, Carbenicillins, Piperacillin
2. TC is from carboxypenicillin P is from ureidopenicillin
3. Carbenicillin was d/c b/c of the high Na load. Ticarcillin is more potent so less drug needed and less Na

Front 5

1. What is ticarcillin (a carboxypenicillin) given in combination with?
2. Mnemonic for beta lactamase inhibitors?

Back 5

1. Beta lactamase inhibitor (clavulanic acid)
2. CaST: Clavulanic acid (with amoxicillin, Ticarcillin) Sulbactum (Ampicillin) & Tazobactam (Piperacillin)

Front 6

1. How do cephalosporins work?
2. What is the activate part of the cephalosporin?
3. How is it different from a penicillin?

Back 6

1. Block peptidoglycan cross-linkage (gram + and -), activate autolytic enzymes in gram +
2. Has a 6-membered dihydrothiazine ring, can accept substitutions at 2 locations (penicillins - only 1)

Front 7

1. What are the first generation of cephalosporins useful against?
2. What are the oral drugs from the first generation?
3. Paraenteral?

Back 7

1. PEcK - Proteus mirabilis, Escheriichia coli, Klebsiella pneumoniae (all aerobic gram + organisms)
2. Cephalexin
3. Cefazolin

Front 8

1. What are the second generation of cephalosporins useful against?
2. What are the oral drugs from the first generation?
3. Paraenteral?

Back 8

1. HEn PEcK - Haemophilus influenzae, Enterobacter aerogenes, Proteus mirabilis, Escheriichia coli, Klebsiella pneumoniae (mostly aerobic gram + organisms, but one gm -, the enterobacter)
2. Cefuroxime axetil
3. Cefuroxime,

Front 9

1. What is a second generation cephamycin?
2. Bacteria it is effective against?
3. What are the oral drugs from the first generation?
4. Paraenteral?

Back 9

1. Has a methoxy-group at position 7
2. many gram (-) anaerobic bacteria
3. None
4. Cefoxitin, Cefotetan

Front 10

1. What was the benefit of the 3rd generation of cephalosporins?
2. What specifically was it more effective at treating?
3. Which 3rd generations are parenteral?
4. Oral?
5. What is an antipseudomonal?

Back 10

1. Resistant to many beta lactamases which increased activity against many gram - orgs.
2. Meningitis caused by susceptible bacteria, mb better at crossing the BBB
3. Cefotaxime & ceftriaxone
4. Cefixime
5. ceftazidime

Front 11

1. What is the e.g. of the 4th generation cepthalosporin?
2. What is it more useful?
3. How is the drug given?

Back 11

1. Cefepime
2. Works well against gm + and gm - bacteria, but can't cross the BBB well so no meningitis
3. Paraenteral (IV/IM)

Front 12

1. what is the e.g. of the 5th generation cephalosporin?
2. Why is it useful?

Back 12

1. Ceftaroline (paraenteral)
2. Works against multidrug resistant Gram + bacteria. Administered as a prodrug (has to be activated)

Front 13

1. What do N-methylthiotetrazole rings do to clotting?
2. to alcohol processing?
3. Which class of drugs might have these rings?

Back 13

1. decrease platelet agregation by decreasing K+ dependent synthesis of prothrombin
2. decreases alcohol tolerance by inhibiting the enzyme that converts acetaldehyde to acetate leading to nausea, vomiting etc
3. Cephalosporins (cefotetan)

Front 14

1. What is the distinguishing factor of monobactams?
2. What is the name of the drug?
3. Why is it useful
4. How is it given?

Back 14

1. Monocyclic beta lactam ring
2. Azreonam
3. resistant to many beta lactamases, but not against gram + or anaerobes, very unallergic
4. IV

Front 15

1. What is the distinguishing feature of carbapenems?
2. What are the 4 members of the group?
3. How are they all given?
4. What do they work against?
5. Not work against?

Back 15

1. Lack sulfur in 5 membered ring
2. DIME - Doripenem, Imipenem, Meropenem, Ertapenem
3. All given paraenteral only
4. Broad spectrum (gram +, -, anaerobes & pseudomonas a
5. VRE, MRSA

Front 16

1. What drug classes does Carbapenemase give resistance to?
2. What drug classes does NDM-1 give resistance to?

Back 16

1. All beta lactams
2. all antibiotics

Front 17

1. Why is imipenem (a carbapenem) given combined with cilastatin?
2. Why are the other 3 carbapenem's immune to this?

Back 17

1. If not, it is hydrolyzed in the brush border of the proximal tubule and forms nephrotoxic metabolites. Cilastatin prevent this
2. a methyl group gives stability against hydrolysis (by DHP I)

Front 18

1. What are the 4 stages that antibiotics work against?
2. Type of antibiotic it vancomycin? What stage does it work against?
3. How does it work?

Back 18

1. Synthesis, Export, Assembly, cross-linking
2. Glycopeptide antibiotic, works against assembly
3. It wraps around the D-Ala-D-Ala side chain which prevents transglycosylation of the backbone

Front 19

1. What is the difference between transglycosylation and transpeptidation?

Back 19

1. Glycosylation is the building of the backbone (lengthening) whereas transpeptidation is cross-linking of the chains (strengthening) after they are built

Front 20

1. How is the interaction between D-Ala-D-Ala stabilized?
2. Does vancomycin bind substrate or enzyme?
3. what about beta lactams?
4. How does a bacteria get vancomycin resistance?
5. Why is it effective?

Back 20

1. By 3 hydrogen bonds
2. Substrate
3. Binds the PBP (transpeptidase) enzyme
4. Synthesize a desipeptide with D-Lact rather D-Ala as a terminal end
5. Instead of 3 H bonds being formed, only 2 are possible so binding is not sufficient to block the site

Front 21

Vancomycin blocks transglycosylation because it is huge.
1. due to size what will it work on?
2. How is it gotten rid of?

Back 21

1. Only gram + bacteria, will not get through gram - pores Also will not work in the CNS b/c cannot cross BBB
2. It can't be metabolized by P-450 so only by excretion through urine

Front 22

1. How is vancomycin given?
2. Why would you give it?

Back 22

1. IV ... only oral if there is something in the GI you want to kill
2. Serious Gram + infections that are resistant or patient has penicillin hypersensitivity. Also MRSA NOT MSSA

Front 23

1. What are side effects of Vancomycin?

Back 23

1. GIAR (GLycopeptide induced anaphylactoid reaction) direct effect on mast cells to release. use dilute solutions and infuse slowly to prevent risk.
2. Nephrotoxicity
3. Ototoxicity