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*MOD I Exam 3 > Intro to Antibiotics > Flashcards

Intro to Antibiotics Flashcards

1
Q

How do glycopeptdes and lipoglycopeptides differ mechnistically from the beta lactams?

A

- Beta lactams bind to an inhibit transpeptidase

  • Glycopeptides and lipoglycopeptides bind the cell wall precursors and prevent cell wall cross-linking and extension
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2
Q

Which antibiotic relies on the renal dipeptidase inhibitor, celastatin?

A

Imipenem

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3
Q

What differentiates second generation cephalosporins from cephamycins?

A
  • The bacterial spectrum
  • Cephamycins are active against B. fragils and some Serratia spp.
  • Second generation cephalosporins (cefaclor, cefprozil, and cefuroxime) are NOT
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4
Q

What is the general spectrum of coverage for the monobactam, aztreonam?

A

Gram-negative, aerobes

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5
Q

What is the difference in MOA between oxazolidinones and streptogramins?

A
  • Oxazolidinones bind to the P site on the ribosome and prevent initiation of protein synthesis
  • Streptogramins have a two-headed mechanism as they are given clinically in a combine ratio (30% quinupristin and 70% dalfopistin)
  • Quinupristin inhibits polypeptide elongation and induces early termination of protein synthesis
  • Dalfopistin impedes the polypeptide chain formation and induces conformational change in the 50S ribosomal subunit that enhances quinupristin binding!
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6
Q

Why are the macrolides grouped w/ the ketolides?

What distinguishes a macrolide from a ketolide?

A
  • Grouped together because of similar MOA, chemical structure, and adverse effects
  • Their bacterial coverage differs, Ketolides can be active in macrolide resistant strains
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7
Q

What is the MOA for Penicillins?

What must bacterial cells be doing in order for Penicillin to be effective?

A
  • Interfering w/ the transpeptidase (peniciilin-binding protein) rxn, which inhibits peptidoglycan cell wall crosslinking and leads to a lack of cell wall rigidity
  • Only kill bacterial cells when they are actively growing!
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8
Q

What are the 4 bacterial mechanisms for resistance to Penicillins?

A

1) Beta lactamases
2) Alteration of porin channels (porins are the gateway for penicillins to access the cell wall in a gram-negative bacteria)
3) Altering molecular structure of PBP/transpeptidase (point mutation in binding pocket)
4) Upregulation of efflux pumps (actively transports penicillin out of cell)

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9
Q

Penicillin G has its greatest bacterial coverage against?

A
  • Gram-positive cocci (**S. pneumoniae, S. pyogenes, and Viridans group Streptococci)
  • Certain Gram-negative cocci
  • non-β-lactamase-producing anaerobes (C. perfringens)
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10
Q

Aminopenicillins were created for improvement of?

Their expanded coverage is attributed to?

A
  • Gram negative coverage
  • Increased binding affinity to transpeptidase/PBP and increased penetration through the outer membrane of gram negative bacteria
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11
Q

Aminopenicillins cover gram positives and what major gram negatives?

A
  • E. coli
  • The enterics (Proteus, Salmonella, Shigella etc..)
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12
Q

Combination with what improves the effectivness of Aminopenicillins?

A

Beta-lactamase inhibitors

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13
Q

What are the 4 drugs that fall in the class known as Penicillinase resistant penicillins?

A

1) Methicillin
2) Nafcillin
3) Oxacillin
4) Dicloxacillin

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14
Q

What is the one key difference in bacterial mechanisms of resistance to penicillinase resistant penicillins?

Specifically this class of drugs is resistant to the penicillinase produced by?

Can resistant phenotypes still arise?

A
  • They are less susceptible to penicillinase (beta lactamase) when compared to other penicillins
  • Specifically they are resistant to the penicillinase produced by staphylococcal specices (S. aureus and S. epidermidis)
  • -* Resistant phenotypes can still arise as seen in development of MRSA and methicillin resistant S. epidermidis (MRSE)
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15
Q

What is considered the primary antibiotic for staphylococcal infections once methicillin resistance has been ruled out?

A

Penicillinase resistant penicillins

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16
Q

Ticarcillin, carbenicillin, piperacillin, and mezlocillin belong to what antibiotic drug class?

A

Anti-pseudomonal penicillins

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17
Q

Which antipseudomonal penicillin is the only one in the drug class still used clinically in the US?

A

Piperacillin

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18
Q

Which antibiotic has the broadest spectrum out of all other penicillins?

A

Piperacillin

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19
Q

What was the main aim in the creation of the antipseudomal penicillins, why?

A
  • To make a penicillin that would cover P. aeruginosa, due to it being resistant to many differnt antibiotics
  • Another goal, was to expand penicillin gram negative coverage
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20
Q

What is the MOA of action for Cephalosporins; work best when?

How are they different from penicillins in regards to resistance and coverage?

A
  • Almost identical MOA as penicillins; work best in rapidly proliferating bacteria
  • Although, they can be degraded by beta-lactamases, they are more stable to many beta-lactamases that would degrade penicillins
  • Tend to have broader spectrum of activity versus penicillins
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21
Q

What are the 4 bacterial mechanisms of resistance to Cephalosporins?

A

1) Beta-lactamases
2) Altering porin channels (preventing cephalosporin from entering the gram negative cell to inhibit cell wall synthesis)
3) Altering cephalosporin binding to transpeptidase due to point mutations in the cephalosporing binding pocket
3) Increased efflux of cephalosporin out of the cell

*Same mechanism used against penicillin!

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22
Q

What is the general rule for cephalosporin coverage by the first, second, and third generation classes?

A
  • First generations have better gram positive coverage (i.e., S. aureus)
  • Second generations fall in the middle and provide ok coverage for both gram positive and gram negative
  • Third generations have better gram negative coverage (i.e., E. coli)
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23
Q

What is the most common side effect to Cephalosporin?

A
  • Just like penicillin, hypersensitivity to the beta lactam ring
  • Most common manifesting as a maculopapular rash developing several days after therapy

*A hypersensitivity reaction to cephalosporin would likely have cross reactivity to penicillin, due to the structural similarities. Important to note so that you can avoid these drugs if allergy of either is known.

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24
Q

Cefazolin and cephalexin belong to what antibiotic class?

A

First generation cephalosporins

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25
Q

First generation cephalosporins are known for their acitivity against which bacteria?

What are the exceptions?

A
  • Gram positive cocci such as S. aureus
  • Most gram-positive cocci are susceptible
  • Main exceptions include MRSA, enterococci, and S. epidermidis
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26
Q

Cefuroxime, cefaclor, and cefprozil belong to what antibiotic class?

A

Second-generation cephalosporines

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27
Q

Cefotetan and cefoxitin belong to what antibiotic class?

A

Second generation cephalosporins known as cephamycins

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28
Q

Second generation cephalosporins should not be used to treat which bacteria due to the increased propensity to select for resistant mutants that posses constitutive expression of beta lactamases.

A

Enterobacter spp

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29
Q

Which adverse effects may be produced by the cephamycin (second generation cephalosporin), Cefotetan?

A
  • Hypoprothrombinemia and bleeding due to the methylthiotetrazole ring on its structure
  • Also, due to this ring, cefotetan can elicit a disulfiram-like reaction, therefore alcohol must be avoided
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30
Q

Cefotaxime, cefixime, cefdinir, ceftibuten, ceftazidime, ceftriaxone, cefpodoxime proxetil, and cefditorem pivoxil are antibiotics in what class?

A

Third generation cephalosporins

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31
Q

What is the only third generation cephalosporine that is active against P. aeruginosa?

A

Ceftazidime

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32
Q

What are 2 of the important side effects produced by an antiobiotics in the third generation cephalosporin class?

Which antibiotic specifically?

A
  • Ceftriaxone may displace bilirubin due to its high binding affinity for serum albumin —> jaundice in neonates
  • Also has a high affinity for calcium, and may also lead to biliary pseudolithiasis (i.e., gallstones)
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33
Q

Cefepime belongs to what class of antibiotics?

A

Fourth generation cephalosporin

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34
Q

Although, fourth generation cephalosporins (cefepime) are bacterially resisted like the other cephalosporins these drugs are resistant to certain beta lactamases, what are they?

Allows it to exhibit activity against which bacteria?

A
  • AmpC beta lactamases
  • Activity in Enterobacter spp. and Pseudomonas spp.
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35
Q

The fourth generation cephalosporins provide what type of bacterial coverage?

A

Expanded gram-negative coverage: P. aeruginosa, Entrobacter spp. (EXCELLENT coverage), and most gram positives

36
Q

Ceftraroline fasamil and ceftolozane are part of what antibiotic class?

A

Fifth generation cephalosporines

37
Q

The fifth generation cephalosporine, ceftazidime is normally found co-formulated with?

A

Beta-lactamase inhibitor tazobactam

38
Q

Fifth generation cephalosporins really shine when it comes to tough bugs like?

A
  • Ceftaroline is active against MRSA and penicillin-resistant S. pneumoniae
  • Ceftolozane against Pseudomonas spp. and is co-formulated w/ beta-lactamase inhibitor tazobactam to provide increased activity against enterobacteriaceae (GRAM NEGATIVES)
39
Q

Imipenem, meropenem, doripenem, and ertapenem are part of what antibiotic class?

A

Carbapenems

40
Q

What is the clinical relevancy of imipenem?

A
  • First drug of the Carbapenem class and tends to have more adverse effects
  • Requires combination w/ a renal dipeptidase inhibitor, celastatin, in order to maintain clinically relevant concentrations in the body
41
Q

Carbapenems tend to be relatively resistant to what?

Other than the mechanisms bacteria use to resist penicillin and cephalosporins, what is another way they may have reistance to these drugs?

A
  • Relatively resistant to degradation by beta lactamases
  • Batceria can upregulate enzymes to degrade carbapenems, called carbapenemases, which degrade the drugs structure
42
Q

Carbapenems as a class are good agents for targeting?

A

Gram-negative bacteria

43
Q

Aztreoname belongs to what antibiotic class?

What is unique about this class?

What MOA does this class have?

A
  • Monobactams
  • Have a monolytic beta lactam ring
  • Cell wall inhibitor, like penicillins and cephalosporins
44
Q

Vancomycin is part of what class of antibiotics?

Telavancin, dalbavancin, and oritavancin are part of what class?

A
  • Glycopeptides
  • Lipoglycopeptides
45
Q

Monobactums cover which bacteria class?

A major use of this class of antibiotics is what?

A
  • Gram negative and aerobes
  • Major use = tx of gram-negative infections in pts that cannot tolerate other beta lactam drugs due to an allergy
46
Q

What is the MOA for glycopeptides vs. lipoglycopeptides antibiotics?

A

- Glycopeptides are cell wall synthesis inhibitors and bind to the D-alanyl-D-alanine terminus of cell wall precursor units w/ high affinity. Leading to inhibition of transglycosylase

- Lipoglycopeptides improve on this process by dimerizing and embedding their lipid structures into the bacteral cell membrane. Allows for improved binding to the D-alanyl-D-alanine terminus and increased potency

47
Q

Oritavancin and telavancin (lipoglycopeptides) have a more rapid cidal effect how?

A

Directly disrupt the bacterial membrane

48
Q

What bacterial method of resistance exists for the glycopeptides antibiotics?

A

Changes to the glycopeptide binding site, which is located on a transposon, and allows site to change from D-alanyl-D-alanine –> D-lactate or D-serine

49
Q

Glycopeptide and lipoglycopeptides have affects on what bacterial class?

A

Gram-positive bacteria

50
Q

How must glycopeptides and lipoglycopeptides be administered, why?

A
  • Are poorly absorbed after oral administration, will just sit in the gut
  • Must be given by IV
51
Q

Clavulanic acid, sulbactam, and tazobactam are part of what antibiotic class?

A

Beta lactamase inhibitors

52
Q

Which antibiotic is always co-formulated with the beta lactamase inhibitor tazobactam and why?

A

Piperacillin to give it the best possible gram-negative coverage

53
Q

Linezolid and tedizolid are part of what class of antibiotics?

A

Oxazolidinones (protein synthesis inhibitors)

54
Q

What is the MOA of Oxazolidinones?

Bactericidal or bacterostatic?

A
  • Protein synthesis inhibitor –> bind to the P site on the 50S ribosomal subunit. Preventing formation of the (fMet) tRNA complex.
  • Primarily bacteriostatic, however are bactericidal against streptococci
55
Q

What are the bacterial mechanisms of resistance to Oxazolidinones?

A
  • Point mutations on the 23S rRNA (binding site) on the 50S ribosomal subunit
  • Methyltransferase that can modify th ribosome and alter binding
56
Q

Oxazolidinones are active against majority of what type of bacteria?

A

Gram-positive

57
Q

What are the 3 different categories of adverse effects caused by oxazolidinones?

A

1) Myelosuppression, and most commonly thrombocytopenia (mainly linezolid)
2) Mitochondrial toxicity: lactic acidosis, optic neuritis, and perirpheral neuropathy (mainly >6 wks use of linezolid)
3) Drug-drug interactions: weak inhibitor of MAO –> avoid andrenergic or serotonergic agents (SSRIs) can cause serotonin syndrome (linezolid)

58
Q

Erythromycin, clarithromycin, azithromycin, and fidaxomicin are part of what class of antibiotics?

Telithromycin?

A
  • Macrolides
  • Telithromycin = Ketolide
59
Q

What is the MOA for macrolides and ketolides?

Bacteriostatic or bactericidal?

A
  • Protein synthesis inhibitors –> bind reversibly to the 50S ribosomal subunit and prevents translocation of the tRNA from the A-site to P-site
  • Can also elicit a confomational change in the bacterial ribosome which can result in indirect inhibition of transpeptidation
  • Can inhibit the formation of the 50S ribosomal subunit
  • Are bacteriostatic, but bactericidal at high enough concentrations
60
Q

What are the 4 mechanism of bacterial resistance to macrolides and ketolides?

A

1) Active drug efflux
2) Production of methylase which shields th ribosome
3) Degradation of the drug itself
4) Mutations in the 50S subunit can occur

61
Q

Which antibiotic used to tx C. difficile colitis?

A

Fidaxomicin (macrolide)

62
Q

Macrolides and ketolides are active against what main bacteria?

A

Streptococci, pneumococci, staphylococci

63
Q

Quinupristin and dalfopristin are part of what antibiotic class?

How are they available clinically?

A
  • Streptogramins
  • Dalfopristin = Streptogramin A
  • Quinupristin = Streptogramin B
  • Only available in a combined ratio of 30% q and 70% d
64
Q

What is the MOA for streptogramins; how do they work in synergy?

A
  • Quinupristin inhibits polypeptide elongation and induces early termination of protein synthesis
  • Dalfopristin binds 50S ribsosomal subunit, at a site nearby the quinupristin site, inducing conformational change and enhancing the binding of quinupristin + impedes polypeptide chain formation
65
Q

What are the 3 bacterial mechanism of resistance to Streptogramins?

A

1) Enzymatic inactivation of dalfopristin
2) Altering quinupristin binding site
3) Both drugs can be subjected to active drug efflux

66
Q

Streptogramins are active against what class of bacteria?

A
  • Gram-positives
  • Important to note this combo is inactive against gram-negatives
67
Q

Tigecycline belongs to what class of antibiotics?

A

Glycylcyclines

68
Q

What is the MOA for tetracyclines and glycylcylines?

Bactericidal or bacteriostatic?

A
  • Bind the 30S ribosomal subunit and prevent aminoacyl tRNA from entering the acceptor (A) site; inhibits protein synthesis by indirectly blocking polypeptide elongation
  • Bacteriostatic
69
Q

What are the 3 mechanisms of bacterial resistance to tetracyclines and glycylcyclines?

A

1) Reduced intracellular concentration of the drug due to reduced influx or increased efflux (glycylcylines can resist the efflux sometimes)
2) Upregulation of protein that dislodges the drugs from their target
3) Can be enzymatically inactivated

70
Q

What types of bacteria do tetracyclines and glycylcyclines provide coverage for?

A
  • Tetracyclines: broad-spectrum, but more active against gram + and anaerobes
  • Glycylcyclines: same as tetra w/ added activity against some bacteria that have resistance to tetracyclines
71
Q

Streptomycin, gentamycin, tobramycin, amikacin, neomycin, paromomycin, kanamycin, and netilmicin are part of what class of antibiotics?

A

Aminoglycosides

72
Q

What is the MOA for aminoglycosides? (hint: there are 3 of them)

A
  • Bind to the 30S ribosomal subunit and act as irreversible inhibitors of protein synthesis by:
    1) Inhibiting initiation by fixing the 50S and 30S subunits to the AUG start codon on the mRNA
    2) Inhibit continuation of translation by inhibiting formation of 70S complex
    3) Introduce errors into protein synthesis (i.e., incorrect AAs)
73
Q

Aminoglycosides are bacteriostatic or bactericidal?

A

BACTERICIDAL!

74
Q

Transport of aminoglycosides into bacteria is enhanced by?

A

Cell wall active antibiotics such as: penicillin and vancomycin

75
Q

What are the 3 distinct mechanisms in which bacteria can be resistant to aminoglycosides?

A

1) Enzymatic inactivation (most common) - modify structure thru phosphorylation, acetylation, or adenylation
2) Mutation or deletion of porins inhibiting entry into gram-negatives
3) Mutations of the 30S ribosomal subunit

76
Q

The spectrum of aminoglycosides mainly consists of antibacterial activity against?

A

Aerobic gram-negative bacteria (i.e., Enterobacter, E. coli, Klebsiella, Pseudomonas, Serratia spp.)

77
Q

Antibiotics ending in the suffix “-oxacin” belong to what group?

A

Fluoroquinones

78
Q

What proteins do fluoroquinolones inhibit (MOA)?

A

Topoisomerase II (DNA gyrase) and topoisomerase IV

*DNA/RNA synthesis inhibitors!

79
Q

What is the primary MOA of fluoroquinolones antibacterial action in gram-positive bacteria?

Gram negative?

A
  • Inhibition of DNA gyrase is primary method for gram-negative
  • Inhibition of topoisomerase IV is primary method for gram-positive
80
Q

What mechanisms of bacterial resistance exist for fluoroquinolones?

A
  • Mutations to the quinolone binding region on either DNA gyrase or topoisomerase IV
  • Active drug efflux
  • Least common = upregulation of proteins that protect and shield both DNA gyrase and topoisomerase IV
81
Q

Why are sulfonamides and benzylpyrimidine synergistic?

A
  • Inhibit subsequent steps in the tetrahydrofolate biosynthetic pathway

- Trimethoprim is potent and selective competitive inhibitor of bacterial dihydrofloate reductase

  • Sulfamthoxazole is structural analog of PABA and acts as a competitive non-functional mimic of PABA to inhibit dihydropteroate synthase
82
Q

What class of antibiotics does sulfamethoxazole belong to?

Trimethoprim?

A
  • Sulfonamides
  • Benzylpyrimidines
83
Q

What are mechanisms of bacterial resistance to sulfonamides and benzylpyrimidines?

A
  • Changes to the bacterial tetrahydrofolate biosynthetic pathway
  • Sulfamethoxazole resistance can develop due to bacterial overproduction of PABA (outcompetes the drug) or reduced binding to dihydropteroate synthase or decreased entry into the cell
  • Trimethoprim resistance due to reduced bacterial permeability or upregulation of dihydrofolate reductase or mutations in dihydrofolate which reduce binding
84
Q

TMP/SMX is used to treat what bacterial infections?

A

Many kinds, but notabl is MRSA and P.jiroveci pneumonia

85
Q

What are the MOA for polymyxins?

A
  • Are strongly attracted to the phospholipid bilayer that makes up outer membrane of gram-negative bacteria and act as cationic detergents, disrupting the membrane
  • Bind to and inactivate endotoxin, preventing its release into circulation, preventing fever, diarrhea, and potential endotoxic shock (i.e, septic shock)
  • Are bactericidal
86
Q

Polymyxins are used for antibiotic coverage of which bacteria?

Why only one type?

A
  • Gram-negative ONLY, primarily aerobes
  • Gram positives do not posses an outer membrane

*MOD I Exam 3 (16 decks)

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