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Pharm 2 Part 3: Chemotherapy and Antibiotics and Antifungals > Pharm: L26: Cephalosporins > Flashcards

Pharm: L26: Cephalosporins Flashcards

1
Q

Cephalosporins: Mechanism of Action?

a. Similar to what?

A
  1. Activate cell wall Autolytic Enzymes through BLOCKING of TERMINAL CROSS-LINKING of PEPTIDOGLYCAN
    a. to Penicillins and they also have a Beta-Lactam Ring
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2
Q

Cephalosporins: What’s the big advantage of them over Penicillins?

A

They are ALL NATURALLY RESISTANCE to PENICLLINASE!

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3
Q

Caphalosporins

  1. R2 group: What is it?
  2. R1: Affects what?
  3. 7-Methyl GROUP in Cephalosporins seems to do what?
A
  1. Substitutions DETERMINE degree of Antibacterial Activity
  2. Affects Pharmacokinetic Properties
  3. Seems to Increase their Resistance to B-Lactamase!!
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4
Q

Cephalosporins

  1. First Generation (3) (Cef, and CEPH/CEPH) (AKK)
  2. Second Generation (3)
  3. Third Generation (5)
  4. Fourth Gen (1)
  5. Fifth Gen (1)
A
  1. Cefazolin; Cephalothin and Cephalexin
  2. Cefaclor; Cefuroxime, and Cefprozil
  3. CefoTaxime Sodium; Ceft-ime, Ceft-dime; Ceft-axone; Cefixime
  4. Cefepime (Maxipime)
  5. Ceftaroline (Teflaro)
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5
Q

First Generation Cephalosporins

  1. AKA?
  2. What are the first Gen drugs?
  3. Activity against what bacteria?
  4. Most of what kind of bacteria are SUSCEPTIBLE?
    a. Alternative for what?
  5. Some are resistant to what?
  6. How does the body get rid of them?
  7. Which is the DOC for SURGICAL PROPHYLAXIS? **KNOW THIS!!!
  8. Route of Administration/
  9. Antipseudomonal Activity?
A
  1. Narrow Spectrum cephalosporins
  2. (A: Cefazolin), K (Cephalothin), K (Cephalexin)
  3. Good Activity against G +; moderate against G- Organisms
  4. Most G + COCCI, and MSSA (enterocooci, MRSA and S. Epidermis are resistant)
    a. for Penicillin-Allergic individuals
  5. Some Are ACID RESISTANT; They all have INCREASED B-LACATAMASE RESISTANCE
  6. Renal Excretion
  7. CEFAZOLIN
  8. a. Cefazolin (IV,IM) (Parenteral)
    b. Cephalothin: IV, IM (Parenteral)
    c. Cephalexin: ORAL!!
  9. NO!
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6
Q

Second Generation Cephalosporins

  1. What are the drugs? (3)
  2. Activity levels against G+ and G -?
  3. Antipseudomonal Activity?
  4. Resistant to what?
  5. How does the body get rid of them?
  6. Route of Administration?
  7. Spectrum?

(Really…just know that 1st Gens are a little better at G+ activity, and 2nd Gens are a little better at G- activity and less at G+)

A
  1. CEFACLOR, Cefuroxime, and Cefprozil
  2. Lower Activity against G+; Some INCREASED activity against G-
  3. NO
  4. Some are acid resistant; Increased B-LACTAMASE Resistance
  5. Renal Excretion
  6. a. CEFACLOR (ORAL)
    b. Cefuroxime: IV,IM (Parenteral)
    c. Cefprozil: Oral
  7. Intermediate Spectrum Cephalosporins
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7
Q

Third Generation Cephalosporins

  1. Spectrum level?
  2. What are the six?
A
  1. Broad Spectrum Cephalosporins
  2. a. CEFTRIAXONE (CNS Penetration, Neisseria)
    b. Cefotaxime (CNS Penetration)
    c. Ceftizoxime
    d. Ceftazidime (P. Aeruginosa)
    e. Cefixime (ORAL)
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8
Q

Third Gen Cephalosporins (2)

  1. What 2 drugs have good CNS Penetration?
  2. What drug is the only one that is good against P. Aeruginosa? (good antipseudomonal activity)?
  3. Activity?
  4. What drug is the DOC for N. GONORRHOEAE?
    a. Avoid use in what 2 situations?
  5. Most are excreted from the body how?
A
  1. CEFTRIAXONE and Cefotaxime
  2. Ceftazidime
  3. Less active against G+ and more active against G- (Enterobacteriaceae)
  4. CEFTRIAXONE
    a. Neonates and in Bilirubin Displacement! (Can give to infant w/eye infection caused by Gonorrheae but monitor bilirubin levels)
  5. By the KIDNEY!!
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9
Q

Fourth Gen Cephalosporins

  1. What drugs?
    a. Route of Administration?
  2. Comparable to what Generation of Cephalosporins?
  3. More resistant to what?
  4. ANTIPSEUDOMONAL ACTIVITY?
  5. Activity?
  6. Therapy?
    * As good as it is, it’s not good against MRSA still
A
  1. CEFEPIME
    a. IV
  2. 3rd Gen
  3. to some B-Lactamases
  4. YES!
  5. BETTER G+ Coverage, and BROADEST COVERAGE: (Enterobacteriaceae, MSSA, Pseudomonas)
  6. Empirical Therapy: Esp when resistance to B-Lactamases are anticipated
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10
Q

Fifth Gen Cephalosporins

  1. What drugs?
    a. Route of Administration?
  2. Antipseudomonal Activity?
  3. Only B-Lactam that can treat what?
  4. How does the body get rid of it?
  5. Mechanically, this drug can bind to what?
A
  1. CEFTAROLINE
    a. IV
  2. NO! (One drawback of this drug)
  3. MRSA and VRSA COVERAGE; ONLY BETA LACTAM ACTIVE AGAINST MRSA!!
  4. Renal Excretion
    * Drug of LAST RESORT
    * If she asks us a BETA LACTAM and MRSA QUESTION, THIS IS THE ONLY ONE THAT CAN BE THE ANSWER!!!
  5. to PBP2A w/very high Affinity. This is the mutated PBP that other Beta-Lactams cannot bind to
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11
Q

Cephalosporins: TOXICITY

  1. What is a CONCERN?
    a. What class would you think this is a concern for?
  2. Dilsulfiram-like reaction after alcohol: More likely with what Gen?
  3. ALLERGY: Why would this happen?
  4. What other symptoms?
  5. WHAT IS THE MOST IMPORTANT TOXICITY TO REMEMBER!!!??
A
  1. SUPERINFECTION
    a. 4th GEN (because of BROADER SPECTRUM): Broader the spectrum, the more likely you are to have a superinfection
  2. 3rd Gen
  3. Due to Cross Sensitivity with Penicillins (if you’re allergic to penicillins you may have an allergic reaction with these as well) (10% chance)
  4. GI Symptoms
  5. DOSE DEPENDENT RENAL TUBULAR NECROSIS: Synergistic NEPHROTOXICITY with AMINOGLYCOSIDES
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12
Q

Monobactams

  1. What drugs?
  2. LIMITED TO USE AGAINST WHAT?
  3. Route of Administration?
  4. What is the Advantage to using this drug?
  5. Everything else is the same…
A
  1. AZTREONAM
  2. AEROBIC G- RODS!! (No G+ activity and No activity against Anaerobes)
  3. Parenteral
  4. NO CROSS REACTIVITY with other B-LACATAMS (GOOD FOR PEN ALLERGIC)
  5. 1 B-Lactam Ring; Pretty Resistant to B-Lactamases; Few side effects
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13
Q

Carbpenems

  1. What are they (3: IME)
A
  1. IMIPENEM (given with Cilastatin) (

a It’s inactivated by dihydropentanases in renal tubules; It’s like the idea of adding sulbactam, etc with the penicillins

  1. Meropenem
  2. Ertapenem
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14
Q

Carbapenems: (2): Imipenem and Meropenem

  1. IMIPENEM: Rapidly inactivated by what?
    a. So what must be given with it?
  2. What about Meropenem?
A
  1. Renal Tubule Dihydropepdidases
    a. Cilastatin
  2. Not inactivated by Dihydropeptidases
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15
Q

Carbapenems (3): Imipenem and Meropenem

  1. Route of Administration?
  2. Activity?
  3. What claim do they have?
    a. What can be the concern about this?
  4. What can IMIPENEM cause?
  5. DOC for what?
A
  1. IV
  2. BROAD SPECTRUM (Includes ANAEROBES, G+ AND G- (good for mixed infections))
  3. MOST BROAD SPECTRUM OUT OF ALL THE BETA LACTAMS!!
    a. Superinfections. PSEUDOMONAS may develop resistance RAPIDLY! (Aminoglycoside Combo is Recommended)
  4. HIGH LEVELS can cause SEIZURES!! (Meropenem less likely to cause it)
    a. SO dont give IMIPENEMS to patients w/Renal failure, brain lesions, head trauma, or history of CNS disorders.
  5. B-Lactamase producing Enterobacter Infections!!
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16
Q

Carbapenems (4): Ertapenem

  1. *Big thing to remember: It’s Less Active against what?
  2. Everything else is the same…
A
  1. Against Pseudomonas, so if you suspect this infection, DO NOT USE ERTAPENEM!!
  2. Like the other carbapenems: it’s highly stable against B-Lactamases; Broad spectrum: G+, G-, Anaerobic, esp Enterobacteriaceae.

IV or IM administration!

17
Q
  1. Cell Wall Inhibitor That is NOT a Beta Lactam?
A
  1. VANCOMYCIN!!
18
Q

Vancomycin

  1. What does it do?
    a. Because of this, you can use this against what infection?

b. What else is it good against?
c. How does resistance build up?
2. Route of administration?
a. why?
3. Why is it a drug of last resort?

A
  1. Prevents TRANSPEPTIDATION of the Peptidoglycan chain: Binds to TERMINAL D-ala-D-ala
    a. Against MRSA!!!
    b. USEFUL AGAINST PENICILLIN and MRSA infections, and for Treating G+ INFECTIONS in penicillin-allergic Patients (Parenteral). Effective ONLY IN G+!!
    c. Vancomycin only binds to Alanine, so if the bacteria changes it to something else, Vancomycin won’t recognize it.
  2. Oral
    a. To treat SUPERINFECTIONS caused by STAPHYLOCOCCUS and CLOSTRIDIUM DIFFICILE (First choice: METRONIDAZOL)
  3. Due to emergence of Vancomycin Resistant Enterococci and the need for alternative MRSA treatments
19
Q

Vancomycin (2)

  1. Adverse Effects? (3)
A
  1. OTOTOXIC
  2. NEPHROTOXIC
  3. “RED MAN” SYNDROME (flushing from histamine Release)
    * Aminoglycosides are Ototoxic and Nephrotoxic: so u want to use a protein synthesis inhibitor and an inhibitor of cell wall synthesis together, BUT VANCOMYCIN IS NOT A GOOD CHOICE with Aminoglycosides. (This is why PENICILLINS ARE USED with Aminoglycosides instead)

Pharm 2 Part 3: Chemotherapy and Antibiotics and Antifungals (7 decks)

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