• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/43

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

43 Cards in this Set

  • Front
  • Back
1)Cell wall synthesis inhibitors require...
2)The Beta Lactam Antibiotics are..
3)Beta Lactamases are...

4)Beta lactamase inhibitors
1)actively proliferating bacteria
2)Penicillins, Cephalosporins, Carbapenems

3)bacterial enzymes (Penicillinases, Cephalosporinases) that hydrolyze beta lactam ring on the the beta lactam antibiotics

4)inhibit the beta lactamaze inhibitors and protect penicillins from inactivation
5)Penicillin Binding Proteins are..
6)Transpeptidases are...
7)Why do penicillins have very little toxicity?
8)Main reason for increased level of resistance to Penicillins
5)bacterial cytoplasmic membrane proteins

6)bacterial enzymes involved in cross linking of peptidoglycan chains (if no cross linking, cell wall will be weak and fall apart and will be of no use to bacteria)

7)Because they target the bacterial specific cell wall (mammals dont have cell wall)

8)Being prescribed wrong
Penicillins

1)Structure

2)MOA
2b)How do the bacteria help in penicillins killing of the same bacteria
3)Inactive against organisms without...like...
1)Are derivatives of 6-aminopenicillanic acid and have a B-lactam ring (the R group at end differs in the different penicillns, and decides how it is cleared)

2)inactivate Penicillin Binding Proteins (PBP) by binding covalently AND inhibits Transpeptidases AND makes Autolysins ->Inhibit cross linking (transpeptidation) ->destroying cell wall -> causing cells lysis -> BACTERICIDAL

2b)the bacteria notice the messed up cell wall and produce Autolysin, which hydrolyzes (and breaks down) the peptidoglycan cell wall (in attempt to remodel)

3)Cell Wall; Mycoplasma, Protozoa, Fungi, Viruses
4)Resistance can develop d/t

5)What determines whether penicillin can reach PBP?
6)How do gram pos and gram neg reach the PBPs?
7)Why are penicillins ineffective against Pseudomonas aeruginosa
4)PBP mutations (changes active site and Beta Lactam cant bind)

5)Size, Charge, Hydrophobicity

6)in gram pos, penicillin can easily cross membrane
in gram neg, penicillin must go through porins (channels) to get to PBP

7)pseudomonas aeruginosa is gram negative, but does NOT have channels, so penicillin CANT reach PBP
Penicillin G

1)CU
2)DOC for
3)Resistance?
1)Broad Spectrum
(Gram Pos, Gram Neg, Anaerobic, Spirochetes)

2)Syphillis

3)Any org that makes B-lactamase (thus must give with B-lactamase inhibitor)
Penicillin V

1)Difference from G
1)V is More acid stable than G, thus is given ORAL (V stands for vesco, which in latin means oral)
1)What are the Antistaphylococcal Penicillins?

2)Whats special about them?

3)What are there uses restricted too

4)Which of them is not used clinically?
1)Methicillin, Nafcillin, Oxacillin, Dicloxacillin

2)Are Beta Lactamse RESISTANT

3)only give to B-lactamase producing Staphylococci

4)Methicillin, because is TOO TOXIC (thus never pick Methicillin as answer)
1)Which are the Extended Spectrum Penicillins

2)They are used for?

3)Ampicillin is DOC for
4)Both widely used to treat?
5)Is there resistance with these?
1)Ampicillin, Amoxicillin

2)Gram Positive, and slightly more effective on Gram Negative
3)L. Mono
4)Respiratory tract infections
5)Yes, inactivated by Beta lactamases (thus must give with Beta lactamase inhibitors)
1)What are the Antipseudomonal Penicillins?

2)Active against which bug?

3)Which is most potent of the drugs?

4)Restricted for what infections?
1)Carbenicillin, Ticarcillin, Piperacillin

2)Pseudomonas aeruginosa (special because this gram neg bug does not have the porin to let normal antibiotic through

3)Piperacillin

4)DO NOT GIVE TO ANY RANDOM INFECTION, only P.aeruginosa
1)What are the Repository Penicillins?

2)Why were they deveoped?

3)Penicillin G Procaine given how, and half life?

4)Penicillin G Benzathine given how; and half life?

5)Penicillin G Benzathine good for what problems?
1)Penicillin G Procaine, Penicillin G Benzathine

2)To prolong duration of Penicillin G (inc half life)

3)IM (because of risk of procaine toxicity if given IV); 12 to 24 HOURS

4)IM; 3 to 4 WEEKS (thus only need to give 1 injection and lasts 3 to 4 weeks)

5)Syphillis, Rheumatic Fever Prophylaxis, Strep Pharyngitis (good for these because dont need to dose as often
1)Why give Penicillin and Aminoglycoside together?

2)What should you never do when combining the 2?
1)Synergistic: Penicillin breaks cell wall, allowing aminoglycosides in to do there job

2)Put in the same IV (infusion fluid) because will form an INACTIVE complex
Penicillin Resistance

1)How do you get it?

2)How does ORSA(MRSA) get its resistance (now called ORSA because methicillin not used clinically)
1)Inactivation by B-lactamase
Modification of target PBPs
Impaired Penetration (cant reach PBP)
Efflux

2)Alterged Target PBP (thus beta lactam cant bind
1)Out of all the penicillins, which ones are given only Oral (thus used for Minor Infections)

2)Which of the Penicillins can be given orally or IM/IV

3)Which 2 drugs given only IM
1)Penicillin V
Amoxicillin and Clavulanic Acid
Carbenicillin (the Indanyl Ester form, because it protects it from first pass metabolism)

3)The sustained release Penicillin G Procaine and Penicillin G Benzathine

2)Carbenicillin (the indanyl ester form is given oral; the carbenicillin for is given IV/IM)
1)What impairs the absorption of orally administered Penicillns? What is the Excpetion?

2)Which Penicillin is GI absorption really not effecive?

3)Which drug that is reserved for Beta Lactam resistant Staph is absorbed well Orally
1)Food; Amoxicillin not impaired

2)Nafcillin

3)Dicloxacillin
1)Do penicillins go into CSF well?

2)What 2 organs are penicillins ineffective in?

3)How are most penicillins excreted? What the half life of most?

4)What drug inhibits penicillin excretion?
5)What is the exception to the penicllins that are excreted through kidney, and thus give this drug if have Kidney Disease?
6)Where else are penicillins excreted?
1)NO, unless inflamed in meningitis (then it will go in)
2)Prostate and Eye (cant reach good levels)

3)Through kidney (mostly via tubular secretion, not filtration); 30 min to 1 hour (but if have kidney disease half life can excrete to 20 hours)

4)Probenicid (blocks secretion) (thus get toxic levels of antibiotics) (but also used for advantage, because then can give lower levels of penicillin)(useful on battlefield, when have short supply of penicllin)
5)Nafcillin (is excreted through Bile) (thus if Kidney Disease, GIVE THIS)
6)Breast Milk
1)Why do some patients get hypersensitivity reactions to Penicillins?

2)If allergic to Penicillins,can also be allergic to? Why?
1)The penicillin has Penicilloic Acid (get maculopapular rash->shock) (very rare) (thus if claim to have reaction to penicillins, go with ALTERNATIVE)

2)Cephalosporins; Because both have Beta lactam
Penicillin AE

1)Are?
2)AE assoc with Methicillin
3)AE assoc with Nafcillin
4)AE assoc with Ampicillin, Amoxicillin
5)AE assoc with Oxacillin
5)AE assoc with Ampicillin
1)Diarrhea (all antibiotics can cause this)
Neurotoxicity
Blood Problems
GI Upset, Secondary infections

2)Interstitial Nephritis
3)Nafcillin
4)Maculopapular Rash (will look the same as the hypersensitivity reaction, but is different, doesnt mean are allergic to drug)
5)Hepatitis
6)Pseudomembranous Colitis
1)DOC for Syphillis
2)Bugs Resistant to Penicillin G

3)Use Penicillin V mainly for...
4)DOC for Staph Infections (but these drugs are resistant to?)
1)Penicillin G
2)Pneumococci, S. aureus, N. gonorrhea (but can treat with giving Beta lactamase inhibitor)

3)Oropharyngeal Infections
4)Methicillin, Nafcillin, Oxacillin, Dicloxycillin (ORSA)
1)DOC for Enterococcal Carditis
2)DOC for H. influenzae
3)DOC for Proteus miribalis
4)DOC for Shigella
1-4 = Ampicillin, Amoxicillin
1)The Beta lactamase inhibitors are

2)How do they work?
1)Clavulanic Acid, Sulbactam, Tazobactam

2)They contain Beta lactam ring, but do NOT have antibacterial Activity. (NEVER GIVE THESE ALONE) They bind to and inactivate Beta Lactamases
Cephalosporins

1)Structure
2)MOA
3)resistance?
4)Not active against which 2 bugs?
1)Have a Beta lactam ring, and are derivatives of 7-Amino-cephalosporanic acid
2)Same as penicillins -> BACTERICIDAL
3)Same as penicillins because same MOA (cant switch something that is resistant to penicillin to cephalosporin and expect to work)

4)Enterococci and L. mono
1)What are the 2 First Gen Cephalosporins?

2)are substitutes for what?
3)Resistant to?
4)Are not good at killing?
5)CU for?
1)Cefazolin, Cephalexin

2)Penicillin G (thus if dont have penicillin G, can give these) (but use Penicillin G first)
3)Staph (d/t beta lactamase)
4)B. fragilis

5)Gram Pos, AND P.miribalis, E.coli, and K.pnumoniae
1)What are the 2 Second Gen Cephalosporins?

2)How Differ from first gen?

3)Has Additional Activity again
1)Cefaclor, Cefoxitin

2)Have extended gram Neg coverage (but weaker activity against gram Pos)

3)Enterobacter aerogenes, H. influenzae, Neisseria
3rd Gen Cephalosporins

1)How differ from 1st and 2nd?
2)DOC for?
3)Ceftriaxone or Cefotaxime are DOC for?
4)Ceftazidine with Cefoperazone can work against?
1)Even more effect on gram Neg

2)E. coli
3)Meningitis
4)P. aeruginosa
1)What is the 4th Gen Cephalosporin?

2)How must you give it?
3)CU
1)Cefepime

2)Parenteral
3)Very Wide Spectrum
Cephalosporins

1)Kinetics
2)Which Gen can reach high levels in CSF
3)Which Gen can cross placenta?
4)How are they eliminated?
5)What are the exceptions to elimination?
1)Very Poorly absorbed orally

2)Third Generation
3)ALL GENS
4)mainly Kidneys (thus be careful in patients with Kidney Failure!!)
5)Ceftriaxone and Cefoperazone are excreted in Bile into feces (SO GIVE TO THOSE WITH KIDNEY FAILURE)
Cephalosporins

1)AE
2)AE of giving IM
3)AE of giving IV
4)Which drugs can cause HYPOprothrombinemia? Why? How do you prevent?

5)What else can methyl-thiotetrazole groups cause?
1)Hypersensitivity (same as penicillins, and cross reactivity can occur)
2)Pain at Infection Site
3)Thrombophlebitis
4)Cefamandole, Cefoperazone, Cefotetan; they contain a MEthyl-Thiotetrazole Group; give Vitamin K1 to prevent

5)Disulfiram reactions, thus those drugs also CANT BE GIVEN WITH ALCOHOL (cant break down alcohol)
Cephalosporins (when know not resistant)

1)1st Gen DOC for
2)2nd Gen DOC for
3)3rd Gen DOC for
4)4th Gen used for
1)Surgical Prophylaxis
2)Sinus/Ear/RT infections
3)E.coli/Gonorrhea/S.typhi
4)Gram Neg Orgs (Enterobacter, Haemophilus, Neisseria)
Carbapenems

1)Structure
2)Why special
3)CU
4)Given How? Does it go into CSF?
5)Excreted Though
1)Beta lactam antibiotics
2)Resist hydrolysis by Beta Lactamases

3)Beta lactamase producing Gram Pos and Neg;
P. aeruginosa

4)IV (thus not for minor infections); Yes when inflamed in meningitis
5)Kidney (WATCH FOR KIDNEY PROBS
Carbapenems

5)What are the 2 called?
6)One of them has a bad effect; Which one, and what is effect, and how do you protect against it?
5) Imipenem, Meropenem

6)Imipenem; forms a nephrotoxic metabolite; Give with Cilastatin (thus never give Imipenem alone)
7)General AE of Carbapenems
8)High Levels of Imipenem (mostly d/t renal failure) can cause:
7)N/V/D
Allergic Reactions (some cross reactivity with Penicillins, not as much as cephalosporins)
8)Seizures
9)When do you use Carbapenems

10)Carbapenems are Beta Lactam of Choice for:
9)Only when bug resistant to other drugs
Mixed Aerobic and Anaerobic Infections*

10)Enterobacter infections
Gram Negatives that make Extended spectrum Beta Lactamases
Monobactams

1)What is the 1 drug
2)Structure
3)CU
4)Resistance?
1)Aztreonam
2)Has a beta lactam ring NOT fused to another ring
3)Aerobic Gram Neg Rods (including Pseudomonas)
NO ACTIVITY on GRAM POS or ANAEROBES (THUS IS VERY GOOD CHOICE FOR GRAM NEG INFECTION)

4)Beta lactamases have no effect on it, so can use on Gram Neg that are resistant to other beta lactam antibiotics
Monobactam

1)How is it given?
1)IV/IM (thus NOT for minor infections)

2)GI Upset
Relatively Nontoxic
Little Cross Reactivity (so CAN give if allergic to other Beta lactams)
Vancomycin

1)Structure; STatic or Cidal?
2)Why Special (what bugs used for)
3)CU
1)a bacterial glycoprotein; Bactericidal

2)effective against multi drug resistant orgs (MRSA ENTEROCOCCI) (THUS NOT A FIRST LINE DRUG)

3)Mainly Beta Lactam REsistant Gram Pos (staph)
Strongly allergic PAtients
Vancomycin

4)MOA
5)Why can its MOA be bad?

6)What bugs can you not use for it?
4)inhibits cell wall synthesis and peptidoglycan polymerization (does it by binding to D-ALA-D-ALA terminus of peptidoglycan) (thus prevents CROSS LINKING and ELONGATION) (thus has different effect then penicillins)

5)If even a slight mutation in D-ALA-D-ALA binding site, will become resistant to Vancomycin (D-ALA replaced by D-Lactate)

6)GRAM NEG ORGS (because are intrinsically resistant)
Vancomycin

7)How do you give?
8)What is only time you can give Vancomycin Orally?

9)Does it go into CSF? How is it excreted?
7)Must be IV (slow 60-90 min infusion for systemic infection or prophylaxis) (has very poor oral absorption) (thus another reason only for serious infections)

8)to treat enterocolitis from C. diff

9)YES!; Kidney
Vancomycin

10)AE
11)What AE occurs if drug is allowed to accumulate (eg: kidney failure)

12)If combine with another drug which has same side effect (Aminoglycoside), can cause?
10)Fever, Chills, Phlebitis at infection site (thus give slow administration to get dec risk of having these Side effects)
RED MAN(RED NECK) Syndrome (flushing on face and torso related to high infusion rate)
Hypersensitivity (rash to anaphylaxis)

11)Dose Related HEaring Loss
12)Nephrotoxicity
13)Vancomycin DOC for
14)When cant use Penicillin because allergic, Vancomycin synergistic with Aminoglycoside to treat
13)MRSA(ORSA)

14)Enterococcal Endocarditis
Daptomycin

1)Cidal or STatic
2)CU
3)Does not work against:
1)Bacteriocidal (static at lower conc)
2)Vancomycin Resistant Strains of Enterococci and S. aureus (only used for this)

3)Gram Neg
Daptomycin

4)MOA
5)AE
6)Because of AE, what must u reccommend patient stops?
4)binds to cell membrane via calcium dependednt insertion of kuoud tail -> depolarizes cell membrane with K+ EFFLUX -> Cell death (thus DIFF MOA from rest)

5)GI (all antibiotics have it)
Inc Creatine Phosphokinases

6)Statins (they also elevate Creatine Phosphokinases)
Bacitracin (Neosporin)

1)Structure
2)MOA
3)CU
4)AE; thus used only?
1)Peptide antibioitc

2)interferes with LATE stage cell wall synthesis
3)Gram Pos
Prevent TOPICAL infections of skin

4)MARKED NEPHROTOXICiTY (thus used only Topical)
Fosfomycin

1)MOA
2)CU
1)inhibits EARLY stage of cell wall synthesis by inhibiting cytoplasmic enzyme Enolpyruvate Transferase

2)Gram Pos AND Gram Neg (rare for drug to do this)
Uncomplicated UTI's