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Pharm 2 Part 3: Chemotherapy and Antibiotics and Antifungals > Pharm: L25: Penicillins > Flashcards

Pharm: L25: Penicillins Flashcards

*Know the MOA, (What she covers in lecture is what we need to know). *MOA for all of them. Route of Administration, Adverse Effects, (Broad spectrum, etc) *If she says something more than a couple of times, then KNOW IT!

1
Q

Inhibitors of Cell Wall Synthesis

  1. What structure gives the bacterial cell wall rigidity and resistance to osmotic lysis in G+ and G- bacteria?
    a. What are the major proteins involved in the synthesis of this cell wall structure?
    b. What targets these major proteins?
    c. What is this structure made of?
A
  1. PEPTIDOGLYCAN
    a. Penicillin Binding Proteins (PBPs)
    b. B-Lactam Antibiotics
    c. Backbone of NAD and NAM (sugars that alternate); They have a chain of 4 AAs that extend down the backbones and a PEPTIDE Bride forms b/w them (cross-links the Peptide Chains)
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2
Q

Cell Wall/Peptidoglycan

  1. Major difference b/w Bacterial and Mammalian cells is the presence in bacteria of what?
  2. The Cell Wall protects bacterial cells from what?
  3. In G+, Peptidoglycan is what?
  4. What about G- ?
A
  1. Rigid Cell Wall External to the cell membrane
  2. Osmotic Rupture
  3. it’s the ONLY layered structure External to the Cell Membrane and is THICK (20-80 nm)
  4. There’s an outer membrane external to a thin Peptidoglycan Layer (1 nm)
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3
Q

Peptidoglycan formation

  1. Inhibition of any stage of the SYNTHESIS, Export, or assembly of the Peptidoglycan lead to what?
  2. How is Peptidoglycan formed?
  3. Where do B-LACTAMS act?
A
  1. Inhibition of Bacterial Cell Growth, and usually in CELL DEATH!
  2. Add Subunits (sugar w/5 AAs) that are made in the Cytoplasm. Transport thru cytoplasmic membrane to the cell surface, and Cross-linking occurs that cleaves the Terminal Stem-peptide AA.
  3. On the Peptidoglycan cell wall!
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4
Q

Peptidoglycan Synthesis

  1. Transglycosylation
    a. Formed by what Proteins?
  2. Transpeptidation
    a. Formed by what proteins?
  3. Where does B-Lactams affect this process?
A
  1. Joining NAM-NAG
    a. PBPs
  2. Cross Links Pentapeptides
    a. PBPs
  3. They Bind to the PBPs
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5
Q
  1. What do Glycopeptides do?
    a. What is the name of one of them?
  2. What do B-Lactam Antibiotics do?
    a. Name the B-Lactam classes (4)

b. What inactivates them?

A
  1. Steric Inhibition of adding subunits to the Peptidoglycan Backbone
    a. VANCOMYCIN
  2. Prevent Cross-Linking (TRANSPEPTIDATION)
    a. Penicillins, Cephalosporins, Carbapenems, and Monobactams
    b. Penicillinases and B-Lactamases (Hydrolyze B-Lactam ring thus inactivating the antibiotic)
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6
Q

Lysis and Autolysins (*Know this stuff…she talked about this quite a bit)

  1. What is the MOST IMPORTANT thing to know about killing bacterium with B-Lactams? (what state do they have to be in)
  2. Which antibiotics that inhibit bacterial cell-wall synthesis are Bactericidal?
  3. What is the main cause of Lysis of the Bacterium?
    a. How does this happen?
  4. What PREVENTS the action of Cell Wall Synthesis Inhibitors?
    a. What drug?
A
  1. Have to be in a STATE of GROWTH (if they are STATIC, then they will not work!!)
  2. Basically ALL OF THEM (cuz they lead to Osmotic Lysis)
  3. Lose cell-wall integrity due to their own Remodeling Enzymes (AUTOLYSINS): They cleave the Peptidoglycan bonds during normal cell growth.
    a. When the antibiotics inhibit cell wall growth, AUTOLYSIS still occurs, leading to cell wall weakness and eventual lysis.
  4. Protein Synthesis Inhibitors
    a. Chloramphenicol
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7
Q

What is difficult to treat?

A
  1. Pseudomonas Aeruginosa!
    * Learn these by Groups…
    * Bactericidal
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8
Q

Inhibitors of Cell Wall Synthesis

  1. Agents that Affect the Cell wall? (2)
A
  1. B-Lactam Antibiotics and Other Antibiotics (Bacitracin, Vancomycin, and Daptomycin)
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9
Q

Inhibitors of Cell Wall Synthesis

  1. B-Lactam Antibiotics do what?
A
  1. Inhibit Cell Wall Synthesis, thus they are BACTERICIDAL!!

Penicillins, Cephalosporins, Carbapenems, and Monobactams

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10
Q
  1. What are the 4 B-Lactam Groups?
    a. Why are they called B-Lactams?
  2. What 4 are Not B-Lactams?
A
  1. Penicillins, Cephalosporins, Monobactams, and Carbapenems
    a. They all have a B-Lactam Ring
  2. Vancomycin, Phosphomycin, Bacitracin, and Cycloserine
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11
Q

Penicillins

  1. Natural Penicillins (4)
  2. Penicillinase Resistant (3): NOM
  3. Extended Spectrum (AA)
  4. Antispeudomonal (PTC)
A
  1. PENICILLIN G; Pen V, Procain Pen G, Benzathine Pen
  2. NAFCILLIN, Oxacillin, and Methicillin
  3. AMPICILLIN, Amoxicillin
  4. PIPERACILLIN, Ticarcillin, Carbenicillin
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12
Q

Penicillins: Chemistry

  1. What is the main structural requirement for their activity?
  2. Antibacterial Activity of Penicillin RESIDES in what?
    a. What happens if this is destroyed?
    b. What destroys it?
A
  1. Its nucleus
  2. in the INTACT B-LACTAM RING
    a. Loss of ANTIBACTERIAL ACTION
    b. B-LACATAMASE (PENICILLINASE)
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13
Q

Natural Penicillins

  1. What are they again? (Name the 4)
  2. What is the BIG thing to remember about this group (Have the HIGHEST what?)
    a. Not so good for what bacteria?
    b. What is the trend to remember?
  3. INACTIVATED BY what?
  4. ANTIPSEUDOMONAL Activity?
  5. How does the body get rid of them?
    a. What can be TAKEN with them to help decrease elimination rates?
  6. CNS penestration?
A
  1. Pen G, Pen V, Benzathine Pen, and Procaine Pen G
  2. HIGHEST antibacterial activity against G+ BACTERIA!! (even G+ Anaerobic Bacteria)
    a. not so good for SOME G- Bacteria
    b. As you go down the list of PENICILLINS that she listed, know that Natural Penicillins Have the HIGHEST G + activity, and lowest G- activity, and G+ activity decreases as G- activity Increases moving to the next groups.
  3. PENICILLINASE (B-LACTAMASE)
  4. NONE!
  5. Active Transport in the Kidney
    a. Probenicid
  6. POOR
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14
Q

Mechanism of Action of Penicillins

  1. Type of Antibiotics?
  2. What stage of Cell Wall Synthesis do they INHIBIT?
  3. When are they ONLY BACTERICIDAL?
A
  1. BACTERICIDAL
  2. FINAL STAGE (Cross-linking: Transpeptidation). Bind to PBPs. (PBPs catalyze the RxN that removes the Terminal Alanine to form a crosslink w/the nearby peptide)
  3. ONLY when bacteria are ACTIVELY GROWING and Synthesizing CELL WALLS
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15
Q

Natural Penicillins: Route of Administration

  1. Pen G?
  2. Pen V
  3. Benzathine Pen
  4. Pro Pen G
A
  1. (IV, IM)
  2. Orally useful (tends to be Acid resistant)
  3. IM
  4. IM
    * Works well agains Streptococcus Pneumoniae (but resistance to Pen G has occurred and is increasing); Good against SYPHILIS.
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16
Q
  1. Penicillinase-Resistant Penicillins
  2. What are they? (NOM)
  3. Activity?
  4. BIG THING ABOUT THIS GROUP?
  5. Some of them are what?
  6. DOC for what?
    a. % that is resistant to this drug?
  7. How is it removed?
  8. How do you treat?
    a. What if the drugs don’t work?
  9. Which drug is used for TESTING ONLY!
A
  1. NAFCILLIN, Oxacillin, Methicillin
  2. LOWER ACTIVITY against Certain G + and some G- Coverage
  3. RESISTANT to PENICILLINASE!
  4. Acid Stable and Highly Protein bound!
  5. Penicillinase Producing S. Aureus (MSSA)
    a. More than 20% of S. Aureus (MRSA)
  6. HEPATIC Metabolism and RENAL Excretion
  7. Use NAFCILLIN for a short period of time (IM/IV) then switch to Oxacillin (Oral).
    a. Treat with MAGGOTS! They’ll eat the dead tissue
  8. Methicillin
17
Q

MRSA: Mechanism of Resistance *REMEMBER this INFO!!

  1. Resistance is NOT Associated with what?
  2. What does MRSA produce?
  3. Can a B-Lactam be used to treat MRSA?
    a. What can be used?
A
  1. with the production of B-Lactamase
  2. an ALTERNATE PBP that DECREASES the Affinity of B-Lactam Antibiotics to PBPs
  3. NO!
    a. The only exception is CEFTAROLINE! (5th Gen Cephalosporin)
18
Q
  1. Extended Spectrum Penicillins
  2. Coverage?
  3. ANTIPSEUDOMONAL ACTIVITY?
  4. Does resistance develop frequently?
  5. Susceptible to what?
  6. These drugs are resistant to what?
  7. How are they Excreted?
  8. DOC for what?
  9. What are the drugs and how are they taken?
  10. AMPICILLIN RASH: Is it a Hypersensitivity Reaction?
A
  1. LOWER G+ coverage and EXTENDED G- Coverage!
  2. NO!
  3. YES!
  4. B-LACTAMASE
  5. ACID resistant
  6. Urine
  7. LYSTERIA Infections
  8. AMPICILLIN and Amoxicillin (Oral)
  9. NO!!
19
Q
  1. Antipseudomonal Penicillins
  2. What are they? (PTC)
  3. Spectrum (coverage)
  4. MAJOR USE against what 2 bacteria?
  5. Susceptible to what enzyme?
  6. How are they excreted?
  7. They are sensitive to what?
  8. USE IN COMBO with WHAT?
    a. WHY?
A
  1. PIPERACILLIN, Ticarcillin, and Carbenicillin
  2. Bacteria covered by EXTENDED
  3. P. Aeruginosa (this is the ONLY PENICILLIN THATS ANTIPSEUDOMONAL!) and Acinetobacter
  4. to B-Lactamase (so comibine w/a Penicillinase Inhibitor)
  5. Renal (Kidney) Excretion
  6. Acid Sensitive
  7. with Aminoglycosides
    a. to Prevent Resistance
20
Q

B-Lactamase Inhibitors

  1. There are three of them
    a. Adding them to certain Penicillins will do what?
    b. However…?
A
  1. Sulbactam, Tazobactam, and Clavulanic Acid
    a. They EXTEND the Spectrum of these Agents (so now include organisms resistant by virtue of B-Lactamase production)

b. Not all B-Lactamases are inhibited by these products and bacteria may develop resistance independent upon b-lactamase production (e.g. Altered PBP production and MRSA)

21
Q

B-Lactamase Inhibitors: Combine with what Penicillins

  1. Clavulanic Acid
  2. Sulbactam
  3. Tazobactam
A
  1. Amoxicillin and Ticarcillin
  2. Ampicillin
  3. Piperacillin
    * Not active against MRSA!
22
Q

Bacterial Resistance: Penicillins

  1. Inactivation of penicillin by what?
  2. DECREASED PERMEABILITY of bacterial cell to Penicillins (what Gram bacteria?)
  3. ALTERATION of what?
  4. What enzymes NOT BECOMING ACTIVATED?
  5. LACK of WHAT?
A
  1. Bacterial B-Lactamase (Penicillinase)
  2. Gram -
  3. in PBPs which prevents penicillin from binding (MRSA)
  4. AUTOLYTIC ENZYMES.. Forms “Tolerant” Organisma (Listeria, and Staphylococci)
  5. LACK OF CELL WALL
23
Q

TOXICITY

  1. Highest degree of toxicity?
  2. What 3 other things?
A
  1. ALLERGY (ALL FORMS) (Ampicillin Rash is NOT AN ALLERGY!) (Penicillins and Sulfonamides are the 2 most causes of ALLERGIES)
  2. Electrolyte imbalances, GI Effects (DWAI except for ERYTHROMYCIN has MAJOR GI EFFECTS); Superinfections
24
Q

Pharmacokinetics

  1. What 5 things?
A
  1. Good tissue penetration
  2. Bad CNS Penetration
  3. Mostly excreted via RENAL
  4. Filtration and Tubular Excretion
  5. PROBENECID INHIBITS RENAL ELIMINATION!
25
Q

Ampicillin Rash

  1. How long does it appear?
  2. High % of patients with what disease get this?
  3. RASH IS NOT ALLERGIC!. Does it preclude future use of penicilln?
A
  1. appears 3-14 days after start of therapy
  2. HIGH PERCENTAGE of INFECTIOUS Mononucleosis (EBV)
  3. NO!

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

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