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MICRO_MOA of Antibiotics > MOA_ANTIBIOTICS > Flashcards

MOA_ANTIBIOTICS Flashcards

-See ppt for 1st 8 slides not included -For each of the major classes (penicillins, cephalosporins, glucopeptids, macrolide, tetracyclines, fluoroquinolones, amino glycosides, sulfonamides, trimethoprim) know the MOA and whether the agent is cidal or static

1
Q

Inhibitors of Cell-Wall Synthesis

A

-Beta Lactams
+Penicillins, Cephalosporins, Monobactams Carbapenems

-Glycopeptides
+Vancomycin (Gram+ only)

-Fosfomycin
+UTIs only

-Daptomycin
+Gram+ Only
+4 MRSA, VISA, VRSA, VRE

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2
Q

Beta Lactams

A

Share Beta Lactam Ring

Bactericidal

Nontoxic= Can be administered at high doses

Organic Acids + Most Soluble in H2O

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3
Q

Class of Cell-Wall Inhibitors?

Share Beta Lactam Ring

Bactericidal

Nontoxic= Can be administered at high doses

Organic Acids + Most Soluble in H2O

A

Beta Lactams

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4
Q

PBPs

A

Tranpeptidases that help in peptidoglycan synthesis by catalyzing the final cross-linking reactions of peptidoglycan synthesis

-Two Types: Low and High Molecular Weight

High: involved in different activities during peptidoglycan synthesis

Low MW PBP : D-alanine carboxypeptidases

*Inactivation of Low MW PBPs not thought to affect viability of (bacterial?) cell —-> implications for drug resistance

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5
Q

Beta Lactam Cell Wall Agents

A

Penicillins
6 Different Classes

Cephalosporins
4 different “generations”
Newer class w/ activity against MRSA

Carbapenems

Monobactams (Aztronam)

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6
Q

Describe how beta lactams work.

What are the beta lactams? What class of antibiotics are they?

A

Since beta lactams structurally analogous to D-Ala-D-Ala, PBPs react with these antibiotics (“thinking they are D-Ala-D-Ala) by cleaving the beta lactam bond and forming a stable intermediate that does not react further
+So Beta Lactams acetylate the PBPs and inactivate them

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7
Q

Name specific Penicillin Beta Lactams

A

Natural Penicillins
Pen G

Penicillinase(Beta-Lactamase)-Resistant Penicillins
+resists the bacterial enzyme
Oxacillin, (methicillin, nafcillin + isoxazolyl penicillins)

Extended-spectrum Penicillins
+Aminopenicillins: (ampicillin + amoxicillin)
+Carboxypenicillins (carbenicillin + tiracillin)
+Ureidopenicillins (azlocillin, mezlocillin, piperacillin)

Co-Drugs (Beta-lactam + beta-lactamase inhibitor)

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8
Q

What are some examples of the different generations of Cephalosporin Beta-Lactams?

Generations they belong to?

A

1st generation (narrow spectrum)
Cephalothin, Cefazolin
-most active against streptococci and staphlococci

2nd generation
Cefuroxime, Cefotetan, Cefoxitin
(Haemoph. Influezae)

3rd generation (extended spectrum)
Ceftiaxone, Ceftoxime, Ceftazidime 
\+activity against most Gram- including pseudomonas

4th Generation cephalosporin (extended spectrum)
Cefepime
+activity against most Gram- including pseudomonas

1st gen= better activity against Gram+ and less against Gram-

3rd gen = better gram- negative activity and less gram+ activity

Only 4th agent : broad spectrum both gram + and - activity

3rd and 4th = Extended-Spectrum Penicillin

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9
Q

Example of Cephalosporins that preferentially target Gram+ over Gram- bacteria

A

1st Generation
What are the drugs in 1st Gen Cephs?
Cephalothin and Cefazolin

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10
Q

So patient came in hospital with __Ecoli?___(gram - infection). Which generation of cephlosporin would you use to treat?

A

Third Generation Cephalosporin Treats Gram -
Examples of 3rd Gen Agents:

Ceftiaxone, Ceftoxime, Ceftazidime

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11
Q

Carbepenem Beta Lactams

A

Beta Lactas w/ Broad Spectrum (the Cepime of Cephalosporins)
+active against essentially all pathgenic (and nonpathogenic?) organisms

Effective on Gram+, Except MRSA

Broad Activity agianst Gram-, P. aeruginosa (except Ertapenem) and anaerobes

Slightly diff structure than the other beta lactams
+much more resistant to beta-lactamsse hydrolysis such as ESBL producers

Wide diffusion in the body, esp. in cerebrospinal fluid (CSF)

Examples: imipenem, meropenem, etrapenem, doripenem

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12
Q

Glycopeptides and Lipoglycopeptides

A 
Glycopepitde = another class of cell-wall inhibitors 
   \+Vancomycin

Lipoglycopeptides:
Use for Vancomycin-Resistnat Strains
RX gram+ complicated skin and soft tissue infections
Structurally related to Vancomycin - activity against vancomycin-resistant strains

+Dalbacanicin not FDA approved
+Oritavacin not FDA approved
+Telavancin Not yet FDA Approved
+Teicoplanin: Not FDA Approved in USA but widespread in Europe

Glyco and Lipo = Effective against GRAM+ only. The drugs enter without any problem because peptidoglycan does not act as barrier for the diffusion of these molecules.

Not effective against GRAM NEGATIVES - molecule cannot pass through porins

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13
Q

What are the classes of drugs that are inhibitors of protein synthesis?

A 
-Tetracyclines
     \+Glycyclines a new class of antibiotics derived from tetracycline
  • Aminoglycosides (gentamycin, tobramycin)
  • Macrolides (erythromycim, azithromycin, clarithromycin)
  • Lincosamines (clindamycin)
  • Phenicols (chloramphenicol)
  • Ansamycins (rifampin)
  • Oxazolidiones (Linezolid)
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14
Q

Tetracyclines

A
  • Bacteriostatic
  • Broad Spectrum but Limited Use b/c Resistance Common
  • Primary Treatment for Chlamydiae, Rickettsiae and Mycoplasm
  • Not recommended for children <2yrs and Pregnant women b/c toxicity to bones and teeth of fetus
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15
Q

Why was Glycycline developed?

A

-Developed to Overcome some of the more common tetracycyline resistance mechanisms
-Like Tetracyclne, Bacteriostatic, Broadspectrum
Example: Tigcycle
New Class (of Inhibitior of Protein Synthesis)

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16
Q

Structure Classification and Groups of Tetracyclines

A

Structure: 4 fused 6-membered ring forms the basic structure from which various tetracyclines are made
Classification: Based on Length of Activity in Body and Absorption From GI

Groups:

1: short-actinf (tetracycline, oxytetracycline)
2: intermediate (demeclocycline)
3: long-acting (doxycycline, minocycline)

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17
Q

What class of Antibiotics are Aminoglycosides?

A

Protein Synthesis Inhibitors, Just Like Tetrcyclines (+ Glycyclines)

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18
Q

Aminoglycosides _ MOA?

Toxicity?

A

They are Protein Synthesis Inhibitors
Work By Binding to RNA of the 30S RNA subunit that affects all stages of normal protein synthesis - bactericidal activity

Renal and Ototoxicity; need to monitor blood levels

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19
Q

Examples of Aminoglycosides. How do they work?

A

+Gentamycin, Tobramycin, Amikacin, Streptomycin

They are Protein Synthesis Inhibitors
Work By Binding to RNA of the 30S RNA subunit that affects all stages of normal protein synthesis - bactericidal activity

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20
Q

Macrolides, Lincosamides, Streptogramins, Ketolides

A

Bacteriostatic
Not Broad Spectrum : limited to Gram+ Cocci such as Staphylococci & Streptococci
Also active against anaerobes

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21
Q

Bacteriostatic
Not Broad Spectrum : limited to Gram+ Cocci such as Staphylococci & Streptococci
Also active against anaerobes

A

Macrolides, Lincosamides, Streptogramins, Ketolides

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22
Q

Macrolides

Class? Examples? Uses?

A

Protein Synthesis Inhibitors

Erythomycin, Zithromax Z-Pak (azithromycin)
-respiratory infections due to S. pneumonia and S. pyogenes, Mycoplasms

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23
Q

Lincosamides

Class? Examples? Uses

A

Protein Synthesis Inhibitors

Clindamycin - Gram+ skin Infections

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24
Q

Streptogramins

Class? Examples? Uses?

A

Quinupristin/Dalfopristin (Synercid) Used for E faecalis (VRE) and MRSA

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25
Q

Phenicols: Chloramphenicol

Class?

Use?

Restricted Use?

Toxicity?

A

Protein Synthesis Inhibitors

Broad Spectrum::: Very active against many Gram+ and Gram- bacteria, Chlamydia, Mycoplasma and Rickettsiae

Restricted Use (why?) for extra-intestinal severe salmonella infection

High toxicity, causes Bone Marrow Aplasia and other hematological abnormalities

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26
Q

Oxazolidinones: Linezpid

Class? Use? MOA?

A

Protein Synthesis Inhibitor

Relatively New
Gram+ Infections; Effective For E. Faecium, VRE, MRSA, and multi drug resistant strp pneumoniae

Trade name Zyvox

Linezolid disrupts bacterial growth by inhibiting initiation in protein synthesis

Inhibitors not yet reported?
Gram- bacteria appear to be naturally resistant

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27
Q

Ansamycins>Rifamycins>Rifampin (Rifamipicin)

Class?
Spectrum?
Uses?

Prophlaxsis for?

A

Protein Synthesis Inhibitors

Mostly Gram+, Some Gram -

  • Used in Combination w/ Other Drugs to Treat TB
  • Prophlaxsis in N. Meningitidis Carriers
  • Combo w/ other antibiotics to treat severe Staphylococcal infections (including MRSA)
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28
Q

Inhibitors of Membrane Function?

A

Lipopeptides: Polymyxins and

Cyclic Lipopeptides: Daptomycin

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29
Q

Class of Antibiotics?

Lipopeptides: Polymyxins and
Cyclic Lipopeptides: Daptomycin

A

Inhibitors of Membrane Function

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30
Q

What class are Liptopeptides? Examples?

A

Inhibitors of Membrane Function

-Polymyxin B
High Toxicity - neuro and nephrotoxic (NS and Kidneys)

-Colistin
Narrow Spectrum, For Gram-
Recent Use, Treats Multidrug Resistant Acinetobacter infections
High nephro and neurotoxicity

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31
Q

What class are cyclic lipopeptides: Daptomycin

FDA approved for? By what microorganisms?

A

Inhibitors of Membrane Function

FDA approved for Skin/Skin Structure Infections
+S. aureus (MRSA and MSSA)
+Beta-hemolytic Streptococci (A, B, C, G)
+E. Faecalis (Vanco Sensitive)

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32
Q

FDA approved for Skin/Skin Structure Infections
+S. aureus (MRSA and MSSA)
+Beta-hemolytic Streptococci (A, B, C, G)
+E. Faecalis (Vanco Sensitive)

A

Daptomycin (Inhibitor of Cell Membrane Function)

33
Q

Antimetabolities:Which Pathway do they Inhibit?

Why is the PWAY Impt? Folate essential for synthesis of which bases?

Why is this Pway a good selective target?

Examples of Antimetabolites?

A

Folate Pathway

Makes Adenine and Thymine

Humans do not make folic acid. Good selective target.

Examples: Sulfonamides and Trimethoprim/Sulfamethoxazole

34
Q

The ff are examples of what class of Antibiotics?

Sulfonamides and Trimethoprim/Sulfamethoxazole

A

Antimetabolites

35
Q

Sulfonamides

Class?

Cidal or Static?

Treats?

A

Antimetabolites

Bacteriostatic
1st effective systemic antimicrobial agent
Used to treat acute, uncomplicated UTIs

36
Q

Trimethoprim/Sulfamethoxazole

Class of Antibiotic?

A

Antimetabolite

TMP/SXT bactericidal (Bactrim)
Broad Spectrum
Synergistic Action

37
Q

Sulfonamides

Pharmacokinetics
Clinical Uses
Adverse Reaction

A

An Antimetabolite

Pharmacokinetics: Good Urine Solubility, high levels in urine

Uses:
Acute UTIs (a la sulfonamides)
Patient Allergic to Penicillins
Otitis Media

Adverse Reactions:
-Allergies: may lead to Steven-Johnson syndrome
+An immune-complex-hypersensitivity (allergic) condition that affects the skin and mucous membranes
+Incidence of sulfa allergy similar to penicillin (3% of population)
-Ker nicterus
-Hemolytic Anemia

38
Q

Antimetabolite that causes the following Adverse Reactions:

Adverse Reactions:
-Allergies: may lead to Steven-Johnson syndrome
+An immune-complex-hypersensitivity (allergic) condition that affects the skin and mucous membranes
+Incidence of sulfa allergy similar to penicillin (3% of population)
-Ker nicterus
-Hemolytic Anemia

A

Sulfonamides

39
Q

TMX/SXT

Class of Antibiotics?
MOA?

A

Antimetabolite

Resembles a microbial substrate and competes with the substrate for limited microbial enzyme
-Drug ties up the substrate and blocks a step in metabolism

40
Q

Classes and Drug Examples of Inhibitors of Nucleic Acid Synthesis

MOA?

A

Quinolones - 1st Generation - Narrow Spectrum
+Nalidixic Acid, Cinoxacin

Flouroquinolones
+Ciprofloaxin, Levofloaxcin, Norfloxacin, Ofloxacin, Moxifloxacin

MOA: Target Topoisomerases e.g. DNA-syrase, which is responsible for cutting one of the chromosomal DNA strands at the beginning of the supercoiling process

Furanes

41
Q

Class of Drug?

Target Topoisomerases e.g. DNA-syrase, which is responsible for cutting one of the chromosomal DNA strands at the beginning of the supercoiling process

A

Inhibitors of Nucleic Acid Synthesis

42
Q

Difference between Antimetabolites and Inhibitors of Nucleic Acid Synthesis?

A

?

43
Q

Class and Subclass of the following Drugs:

+Ciprofloaxin, Levofloaxcin, Norfloxacin, Ofloxacin, Moxifloxacin

A

Inhibitors of Nucleic Acid Synthesis, Fluroquinolones

44
Q

Furanes

Class?

Spectrum?

Cidal or Static?

Route of Administration?

MOA?

A

Inhibitors of Nucleic Acid Synthesis

Spectrum of Action: UTIs caused by both Gram+ and Gram- Organisms

Broad Spectrum, Bactericidal, Oral

MOA: Damage bacterial DNA. In bacterial cell, nirtofurantoin is reduced by flavoproteins (nitrofuran reductase)
+these reduced products are highly active and attack ribosomal proteins, DNA, respiration, pyruvate metabolism and other macromolecules w/in cell

45
Q

Class of Drugs?

  • Lincosamines (clindamycin)
  • Phenicols (chloramphenicol)
  • Ansamycins (rifampin)
  • Oxazolidiones (Linezolid)
A

Protein Synthesis Inhibitors

46
Q

Class of Drugs?

-Aminoglycosides (gentamycin, tobramycin)
-Macrolides (erythromycim, azithromycin, clarithromycin)
Tetracyclines

A

Protein Synthesis Inhibitors

47
Q

Ker nicterus

A

Sulfonomides (Antimetabolite)

causes this adverse reaction

48
Q

Name 5 features of the ideal antibiotic.

A 
slective target
cidal
narrow spectrum - does not kill normal flora
high therapeutic index - why?
few adverse runs
many routes of admins. (iv, im, oral)
good absorption
good distribution to site of infection
emergence of resistance slow
49
Q

MIC

A

minimum conc of antibiotic which prevents the organism from multiplying (doesn’t necessarily kill the organism)

50
Q

MBC

A

lowest concentration of drug which KILLs the organism

51
Q

T or F

There is a much closer relation ship between the MIC and MBC values for bactericidal drugs that for bacteriostatic drugs

A

True

Why?

52
Q

Depends on Host’s Immune System to eliminate the microorganism

A

Bacteriostatic - describes most antibiotics

53
Q

-Extended Spectrum Beta Lactamases
-Inducible Ampc C Beta-LActamases
-Carbapenase Producing Gram-
-HA and CA MRSA
-Inducible Clindamycin Resistance in Staplococci and Streplococci
-Staphlococci w/ Vancomycin Resistance or Reduced Suceptibility
VRE (Old- But a Resevoir)
Multi Drug Resistant S. Pneumonia (including vancomycin-tolerant strains)

A

Current Challenges

54
Q

Name 5 Current Challenges w/ Antibiotics. Be Specific.

A

-Extended Spectrum Beta Lactamases
-Inducible Ampc C Beta-LActamases
-Carbapenase Producing Gram-
-HA and CA MRSA
-Inducible Clindamycin Resistance in Staplococci and Streplococci
-Staphlococci w/ Vancomycin Resistance or Reduced Suceptibility
VRE (Old- But a Resevoir)
Multi Drug Resistant S. Pneumonia (including vancomycin-tolerant strains)

55
Q

Explain the relationship w/ Toxicity and Effectiveness as it relates to Natural vs. Synthetic Antimicrobial Agents

A

Inverse Relationship between Toxicity and Effectiveness as you move from natural to synthetic antibiotics

Synthetic Antibiotics More Effective and Less Toxic
Natural Antibiotics Less Effective and More Toxic

56
Q

Where do most of out natural Antibacterial Agents come from?

Example of semisynthetic and synthetic antibacterial agents?

A

Fungal Sources
+Ex: Benzypenicillin and Gentamycin

Semisynthetic chemically altered compound:
Ampicillin and Amikacin

Synthetic: Lab
Moxifloacin and Norfloaxin

57
Q

Newer Classes of Antibiotics?

A

Lipoglycopeptides (Telavancin)
Cycliclipopeptides (Daptomycin)
Glycylcyclines (Tigcycline)
Oxazolidinones (Linezolid)

Oxa: Rx MRSA and VRE, Inhibs. Microbial Protein Synthesis

Glycyclines: Rx Gram+ (Incl MRSA), gram -
Similar MOA as tetracycline antibiotics

Cycliclipopeptides (Daptomycin)
Rx Gram+ Infections - including MRSA
MOA: Binds to bacterial membrane and causes rapid depolarization of the cell membrane ; loss of membrane potential leads to inhibition of DNA, RNA and Protein Synthesis

Lipoglycopeptids
Rx Gram+ complicated skin and soft tissue infections
Structurally related to vancomycin - activity against vancomycin-resistant strains

58
Q

MOA? Uses?

Lipoglycopeptides (Telavancin)
Cycliclipopeptides (Daptomycin)
Glycylcyclines (Tigcycline)
Oxazolidinones (Linezolid)

A

Oxa: Rx MRSA and VRE, Inhibs. Microbial Protein Synthesis

Glycyclines: Rx Gram+ (Incl MRSA), gram -
Similar MOA as tetracycline antibiotics

Cycliclipopeptides (Daptomycin)
Rx Gram+ Infections - including MRSA
MOA: Binds to bacterial membrane and causes rapid depolarization of the cell membrane ; loss of membrane potential leads to inhibition of DNA, RNA and Protein Synthesis

Lipoglycopeptids
Rx Gram+ complicated skin and soft tissue infections
Structurally related to vancomycin - activity against vancomycin-resistant strains

59
Q

Static Antibiotics

A

Macrolids (erythromycin), clinadamycin, Sulfsmethoxazole, Trimethoprim, Tetracyclines, Chloramphenicol

60
Q

Cidal Antibiotics

A

Betal Lactams, Vancomycin, Aminoglycosides (gentamycin), Flouroquins (ciprofloxacin)

61
Q

When would you want to use broad spectrum antibiotics?

A
  • Use empirically prior to identifying the causative bacteria when there is a wide differential and
  • Potentially serious illness would result in delay of treatment
62
Q

Broad Spectrum Antibiotics

A

Carbepenems
Extended -Spectrum Cephalosporins
beta-lactm/beta-lactam inhibitor combination
Newer fluroquinolones

Broad Spectrum might kill normal flora?

63
Q

Narrow Spectrum (selective)

A

Older Penicillin Gs, the Macrolides. Vancomycin (only Gram +)

-Narrow spectrum does not kill normal dlora

64
Q

Most Agents In This Class Interfere w/ Murein Assembly and Peptidoglycan Synthesis

A

Cell Wall Synthesis Inhibitors

65
Q

Carbapenams

A

Cidal, Broad Spect, Cell Wall Inhibitor

66
Q

Monobactams

Class?

Organism?

A

Beta Lactam Antibiotics - cell wall synthesis inhibitors

Aztronam

Aerobic Gram- Bacilli

67
Q

How is action of Vancomycin unique w/ respect to beta lactams?

A

Binds D-Ala - D-Ala instead of the PBP —same effect of preventing crosslinking of the peptidoglycan sheets (Cidal)

68
Q

Inhibits phosphoenel pyruvate halting muramic acid synthesis. Indicated in treatment of UTIs, where it is usually administered in a single megadose

A

Fosfomycin, Cell Wall Synthesis Inhibitor

Cidal

69
Q

Interferes w/ Initiation of Protein Synthesis

by binding to 30S Ribosome and Changing its shape so that it inhibits proteins synthesis by causing misreading of RNA

A

Amnoglycosides

Cidal

70
Q

Used to treat SEVERE infections caused by Gram+ bacteria that are resistant to other antibiotics

A

Linezolid (Class?)

-should not be used against bacteria that are sensitive to drugs with a narrower spectrum of activity, such as penicillins and cephlosporins

Blocks Formation of Translation initiation complex by binding the 23S portion of the 50S subunit

Static

71
Q

Blocks Exit of Growing Peptide chain by binding 23S rRNA

A

Macrolids

Static

72
Q

Similar Action as Macrolids

A

Clindamycin

Blocks Exit of Growing Peptide chain by binding 23S rRNA

Static

73
Q

Chloremphenicol

A

Static

Binds Residues in the 23S rRNA of the 50S ribosomal subunit preventing peptide bond formation (substrate binding)

74
Q

Interference w/ Cytoplasmic Membrane Function

A

Polymixins (topical) - cationic detergent-like activity

BAcitracin (topical) - disrupt cytoplasmic membranes

Antifungals: Polyenes (eg amphotericin), Azoles (eg fluconazole), Allyamines (eg terbinafine) - alteration of sterol (ergosterol) structure and function

75
Q

Tetracyclines

A

static

Inhibits bacterial protein synthesis by blocking the attachment of the tRNA-aa to the ribosome 30S subunit (inhibit codon-anticodon interaction)

76
Q

Inhibits Nucleic Acid Synthesis

A

DNA:

cidal:
Quin and Flouroqunolones (ciprofloxacin, levofloxacin, norflxacin); Inhibit DNA gyrases or topoisomerases required for DNA supercoiling

Metronidazole (metabolic cytotoxic products disrupt DNA)

RNA:
cidal:

Rifampin -Binds RNA polymerase and prevent RNA transcription/RNA synthesis

and Bacitracin (topical) - Inhibits RNA transcription

Nucleoside Analogs: Acyclovir (viruses), Zidovudine (retroviruses)

77
Q

Interference w/ Metabolic Activity/Pathways

A

Sulfonamides (static) and Dapsone (cidal): Compete w. PABA, preventing synthesis of folic acid

Trimethoprim (cidal): Inhibit DHFR preventing synthesis of folic acid

78
Q

Used in ratio 1:5

A

Trimethoprim and Sulfamethoxazole (Bactrim)

  • Synergistic Activity
  • UTIs, Otitis Media, Bronchitis, Traveller’s Diarrhea, Shigellosis (bacillary dysentry)
79
Q

Static

Inhibit bacterial protein synthesis by blocking attachment of the transfer RNA-amino acid to ribosome 30S

Inhibitors of Codon-Anticodon Interactions

A

Tetracyclines

MICRO_MOA of Antibiotics (1 decks)

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