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BIIC Cancers and Pharmo > Antimicrobials Part 1 (Cell Wall Synthesis Inhibitors) > Flashcards

Antimicrobials Part 1 (Cell Wall Synthesis Inhibitors) Flashcards

1
Q

What is prophylactic therapy? What groups should you consider for this type of therapy?

A

Pre-treatment to prevent infection in patients with weakened defenses (immunocompromised states).
Used for individuals on immunosuppressive therapy, cancer patients, and in pre-surgical procedures.

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2
Q

What is empiric therapy? How is an antibiotic selected in this case?

A

Treatment of known or probably infection.

Agent selected based on rational judgement and experience, not just “broad spectrum”.

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3
Q

What is definitive therapy? How might this be favored in comparison to empiric therapy?

A

Pathogen’s identity and antibiotic susceptibility is determined.
Compared to empiric therapy, this reduces risk of resistance emerging to broader-spectrum agents.

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4
Q

What are two reasons to choose a narrow-spectrum agent over a broad-spectrum agent?

A
  1. Reduces risk of superinfection and opportunistic infections (C. difficile)
  2. Reduces risk of community resistance development
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5
Q

What are the two ways cell wall synthesis inhibitors weaken the cell wall of bacteria?

A
  1. Transpeptidase inhibition: Disrupts transpeptidase, which catalyzes the formation of cross-bridges between peptidoglycan polymer strands
  2. Autolysin activation: Increases the activity of enzymes critical for breaking down cell wall segments to permit growth and division
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6
Q

Transpeptidase and autolysin are also known as _____.

A

Penicillin-binding proteins

Penicillins bind to them to produce a lytic effect (bactericidal).

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7
Q

Where are penicillin-binding proteins (PBPs) located?

A

On the cell membrane of both gram-positive and gram-negative bacteria.

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8
Q

Do penicillins work on bacteria that lack a cell wall?

A

NO

If bacteria lack a cell wall, they also lack PBPs and therefore, penicillin cannot bind.

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9
Q

What are the three steps in which this class of antibiotics can interfere with peptidoglycan synthesis?

A
  1. Inhibition of synthesis of murein monomers (e.g. fosfomycin)
  2. Inhibition of polymerization of murein monomers into the glycan backbone (e.g. vancomycin)
  3. Inhibition of glycan polymer cross-linking into peptidoglycan (e.g. beta lactams and “others”)
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10
Q

Cell wall synthesis inhibitors are primarily effective against ______ ______ bacteria.

A

Gram-positive

Gram-negative bacteria are intrinsically resistant to many drugs from this class.

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11
Q

Some gram-negative species express ______ _______ permeable to some antibiotics (e.g., ampicillin, amoxicillin, but NOT vancomycin)

A

Porin channels

Note: Some species lack porin channels (Pseudomonas aeruginosa)

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12
Q

What are 3 resistance mechanisms that gram-negative and gram-positive bacteria can acquire/develop?

A
  1. Altered PBPs (e.g. MRSA)
  2. Expression of efflux pumps (e.g. multidrug-resistance protein; Klebsiella pneumoniae)
  3. Beta-lactamase enzymes that degrade beta-lactam drugs (most S. aureus and an increasing number of Streptococci)
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13
Q

The ______ ______ ______ is the common core structure of all beta-lactam drugs which ______ penicillin-binding proteins at the penicillin binding site.

A

Beta-lactam ring, acetylates

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14
Q

The acetylation of penicillin-binding proteins at the penicillin-binding site ______ the enzyme.

A

Inactivates

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15
Q

The spectra and specific properties of beta-lactam drugs vary based on identities of the ______ ______.

A

R groups

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16
Q

Penicillinase, cephalosporinase, and AmpC-lactamase are examples of ______ ______.

A

Beta-lactamases

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17
Q

Which subclass of beta-lactams are largely resistant to beta-lactamases?

A

Carbapenems

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18
Q

Name 4 common beta-lactamase inhibitors

A
  1. Clavulanic acid/clavulanate
  2. Sulbactam
  3. Tazobactam
  4. Avibactam
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19
Q

Beta-lactamases can be inhibited by ______ beta-lactam drugs with other agents

A

Co-administering

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20
Q

Methicillin is an example of how ______ ______ of drug structure can make beta-lactams more resistant to beta-lactamse inactivation

A

Chemical modification

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21
Q

What is penicillin’s principal adverse drug reaction (ADR)?

A

Allergic reactions

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22
Q

Osmotic pressure is ______ inside the bacterial cell membrane and cell wall. Disruption of the cell wall makes the cell favor water ______. A functional cell wall ______ the cell from expanding and bursting. Penicillins ______ the cell wall and cause bacteria to ______ ______ water and ______.

A

High, absorption, prevents, weaken, take up, rupture

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23
Q

What are the three groups of penicillins organized by spectrum of activity?

A
  1. Natural penicillins
  2. Anti-staphylococcal penicillins
  3. Extended-spectrum agents (aminopenicillins and antipseudomonal penicillins)
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24
Q

Natural penicillins are ______ spectrum.

A

Narrow

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25
Q

Natural penicillins target gram-______ organisms and are sensitive to penicillinases.

A

Positive

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26
Q

Clinical uses of natural penicillins (5)

A
  1. Pneumococcal infections (S. pneumoniae) - pneumonia and meningitis (can cross the BBB)
  2. Gonorrhea (Neisseria) - except penicillinase-expressing strains
  3. Gas gangrene (C. perfringens)
  4. Syphilis (Treponema pallidum) - single IM dose is curative
  5. Pharyngitis (beta-hemolytic Streptococcus)
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27
Q

___% of S. aureus strains are resistant to natural penicillins

A

90%

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28
Q

Penicillin G is administered ____ or ____

A

IV, IM

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29
Q

Penicillin V can be administered PO, but use in severe infections is discouraged due to ______ ______.

A

Poor bioavailability

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30
Q

Natural penicillins distribution, half life, and excretion

A

Distributed throughout the body
t 1/2 = 30 minutes
Renally excreted

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31
Q

Benzathine can ______ penicillin G for IM repository (low but prolonged drug levels).

A

Stabilize

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32
Q

Natural penicillins DDIs (1)

A

Anti-gout drug, probenecid, blocks renal transporters and increases penicillin half-life

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33
Q

Natural penicillin considerations

A

Dose adjustment required for patients with impaired renal function

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34
Q

Pediatric dosage of natural penicillins is determined by the child’s ______ ______.

A

Body weight

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35
Q

Natural penicillins ADRs (5)

Otherwise, usually well-tolerated

A
  1. Hypersensitivity (Type I, immediate due to repeat exposure) - 10% of patients self-report an allergy (rash, angioedema, anaphylaxis) to penicillin (contraindication). All other beta-lactams are contraindicated in patients with a previous allergic reaction to penicillin.
  2. Diarrhea: disruption of the normal balance of intestinal microorganisms. Can lead to superinfections caused by C. difficile.
  3. Nephrotoxicity: acute interstitial nephritis
  4. Neutotoxicity: may provoke seizures. Contraindicated in patients with epilepsy.
  5. Hematologic toxicities: decreased coagulation, cytopenias; monitor CBCs
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36
Q

Anti-staphylococcal (penicillinase-resistant) Penicillins Drugs (4)

A
  1. Methicillin
  2. Nafcillin
  3. Oxacillin
  4. Dicloxacillin
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37
Q

Anti-staphylococcal Penicillins Clinical Use

A

Narrow-spectrum agent restricted for S. aureus strains that express beta-lactamases
Also effective treatment for penicillin-susceptible Streptococci and Pneumococci
(MSSA susceptible to this entire class, but MRSA is NOT)

38
Q

Nafcillin and oxacillin route of administration

39
Q

Dicloxacillin route of administration

40
Q

Anti-staphylococcal Penicillins half life and excretion

A

Short half life that requires frequent dosing

Renally excreted, except for nafcillin (biliary excretion)

41
Q

Extended-Spectrum Penicillins (Aminopenicillins) Drugs

A

Ampicillin (IV) and amoxicillin (PO) with same spectrum of activity

42
Q

Extended Spectrum Penicillins (Aminopenicillins) Clinical Uses

A

Broad-spectrum agent effective against some gram-negative organisms (E. coli, H. influenzae, Proteus mirabilis, Salmonella typhi) and most gram-positive organisms

  1. Ampicillin for L. monocytogenes
  2. Amoxicillin for URIs, bacterio-rhinosinusitis, otitis, and LRIs
43
Q

Extended Spectrum Penicillins (Aminopenicillins) Considerations

A

Co-administer amoxicillin/clavulanate or ampicillin/sulbactam to treat strain resistance from beta-lactamases

44
Q

Extended Spectrum Penicillins (Antipseudomonal Penicillins) Clinical Uses

A 
Piperacillin is the only drug of this class in use in the USA
Little gram-positive activity
Primarily targets gram-negative species (Enterobacter, E. coli, H. influenzae, Proteus mirabilis, Proteus [indole positive], Pseudomonas aeruginosa)
Co-administered with tazobactam as combination therapy to broaden spectrum against beta-lactamase-producing organisms (Pseudomonas, Klebsiella pneumoniae)
45
Q

Cephalosporins are ______-resistant drugs that consist of ______ generations

A

Penicillinase, five

46
Q

First Generation Cephlosporins

A

Cefazolin, cephalexin, cefadroxil

47
Q

First Generation Cephalosporins Spectrum of Activity

A

Similar spectrum to anti-staphylococcal penicillins, but better tolerated
Effective definitive therapy against MSSA, streptococcal, and other penicillinase-producing staphylococcal strains (NOT MRSA)

48
Q

First Generation Cephalosporins Clinical Uses

A

UTIs, staphylococcal/streptococcal infections (cellulitis/soft tissue abscesses)
Cefazolin is used for surgical prophylaxis and severe staph infections (bacteremia)

49
Q

First Generation Cephalosporins Excretion

A 
Renal elimination (probenecid can increase half-life)
Dose adjustment required for patients with renal impairment
50
Q

Second Generation Cephalosporins

A

Cefaclor, cefuroxime, cefprozil, cefoxitin, and cefotetan

51
Q

Second Generation Cephalosporins Spectrum of Activity

A

Spectum generally includes organisms susceptible to first generation cephalosporins, plus an extended gram-negative coverage

52
Q

Second Generation Cephalosporins Clinical Uses

A

URIs (sinusitis, otitis media), soft tissue infections, gynecologic infections, perioperative surgical procedures

53
Q

Second Generation Cephalosporins Excretion

A

Renally eliminated (probenecid increases half-life)

54
Q

Third Generation of Cephalosporins

A

Cefotaxime, ceftazidime, ceftriaxone, cefdinir, cefpodoxime

55
Q

Third Generation of Cephalosporins Spectrum of Activity

A

Less potent gram-positive activity (very potent against pneumococci), but have much greater gram-negative activity.
Used to treat serious infections caused by organisms resistant to most other drugs.
Effective against beta-lactamase-producing Haemophilus and Neisseria gonorrhoeae.

56
Q

Third Generation Cephalosporins Pharmokinetics

A

Ceftriaxone t1/2 = 7-8 hours

57
Q

Third Generation Cephalosporins Clinical Uses

A

Ceftriaxone used for severe infections, meningitis, endocarditis
Ceftazidime/avibactam approved for complicated, resistant intra-abdominal or UTIs
Can penetrate body fluids and tissues, including CSF

58
Q

Third Generation Cephalosporins Excretion

A

Renally eliminated, except for ceftriaxone (biliary excretion)

59
Q

Four Generation Cephalosporins

A

Cefepime (IV only)

60
Q

Fourth Generation Cephalosporins Spectrum of Activity

A

Spectrum comparable to 3rd generation, plus Pseudomonas aeruginosa multi-drug resistant strains
More resistant to hydrolysis by beta-lactamases

61
Q

Fourth Generation Cephalosporins Clinical Uses

A

Useful in treatment of Enterobacter infections
Also treats gonorrhea, community-acquired pneumonia, meningitis, UTIs, Lyme disease, and encephalopathy
Distributes well into CSF

62
Q

Fourth Generation Cephalosporins Excretion

A

Renally eliminated

63
Q

Fifth Generation Cephalosporins

A

Ceftaroline (IV)

64
Q

Fifth Generation Cephalosporins MOA

A

Binds to the mutated PBP that confers resistance to almost all other beta-lactams

65
Q

Fifth Generation Cephalosporins Spectrum of Activity and Clinical Uses

A

Active against organisms susceptible to third-generation cephalosporins
Mostly reserved for MRSA

66
Q

Cephalosporins Major ADRs (2)

A
  1. Cross-reactivity with penicillins

2. Some cephalosporins have anti-vitamin K (bleeding) - cefotetan

67
Q

Monobactams

A

Aztreonam (IV or nebulized)

68
Q

Monobactams Spectrum of Activity

A

Narrow-spectrum
No gram-positive activity
Gram-negative spectrum similar 3rd generation cephalosporins
Highly resistant to beta-lactamases

69
Q

Monobactams Clinical Uses

A

Used to treat serious infections (pneumonia, meningitis, and sepsis) caused by susceptible gram-negative pathogens

70
Q

Monobactams Pharmokinetics

A

t1/2 = 1-2 hours
Renally eliminated
Penetrated the BBB

71
Q

Monobactams ADRs

A

Major toxicity uncommon

Skin rashes, elevations of serum aminotransferases

72
Q

Monobactams Considerations

A

Safe for patients with penicillin allergies, EXCEPT ceftazidime

73
Q

Carbapenems

A

Imipenem/cilastatin, doripenem, ertapenem, meropenem

All administered IV

74
Q

Carbapenems Spectrum of Activity

A

Broad-spectrum agents

Important in empiric therapy and against resistant organisms

75
Q

Carbapenems Clinical Uses

A

UTIs, LRIs, intra-abdominal and gynecological infections, skin, soft tissue, bone, joint infections

76
Q

Carbapenems Pharmokinetics

A 
Renally eliminated (70%)
Imipenem/cilastatin t1/2 = 1 hour
Ertapenem t1/2 = 4 hours
Imipenem is hydrolyzed to a toxic metabolite in the proximal tubular epithelium by a renal dipeptidase; cilastatin inhibits renal dipeptidase
77
Q

Cabapenems ADRs

A

Nausea and vomiting common

Cross-reactivity with beta-lactams

78
Q

Glycopeptides

A

Vancomycin, dalbavancin, oritacancin, teicoplanin, and telavancin

79
Q

Glycopeptides Spectrum of Activity

A

Effective against gram-positive organisms and some anaerobes

80
Q

Glycopeptides MOA

A

Inhibits cell wall synthesis by preventing polymerization into glycan strands and prevents cross-linking via transpeptidase (PBP)

81
Q

Glycopeptides Clinical Uses

A

Primary use is Staph/Strep infection in patients with penicillin/cephalosporin hypersensitivities

82
Q

Glycopeptides Pharmokinectics

A

Administered IV
Poor oral distribution (oral formulation limited to treat C. difficile)
Renally excreted

83
Q

Glycopeptides ADRs

A

ADRs are frequent with parenteral administration, though most are minor and reversible
Phlebitis at injection site
Ototoxicity is rare, but dose-related, especially with other ototoxic drugs like aminoglycosides (tinnitus, high-tone deafness, hearing loss, and possible deafness)
Nephrotoxicity is encountered regularly, especially with other nephrotoxic drugs (aminoglycosides)
Histamine-mediated “red (neck) man syndrome” with sudden infusion; can prolong infusion or pretreat with an antihistamine

84
Q

Lipopeptides

A

Daptomycin

85
Q

Lipopeptides MOA

A

Cyclic compounds with lipophilic “tails” that insert into the plasma membrane and disrupt the cell wall through membrane depolarization leading to cell death

86
Q

Lipopeptides Spectrum of Activity

A

Similar to vancomycin
Effective against some gram-positive, vancomycin-resistant strains (VRSA)
Used to treat skin and soft tissue infections, bacteremia, endocarditis

87
Q

Lipopeptides Excretion

A

Renally eliminated

88
Q

Lipopeptides ADRs

A

Can cause myopathy (monitor creatine phosphokinase levels)

Can also cause allergic pneumonitis in patients with prolonged therapy

89
Q

Fosfomycin MOA

A

Inhibits one of the first steps in the synthesis of peptidoglycan by inhibiting enolpyruvyl transferase: prevents formation of UDP-N-acetylmuramic acid, the precursor of N-acetylmuramic acid

90
Q

Fosfomycin Spectrum of Activity

A

Active against gram-positive and gram-negative organisms

Used for uncomplicated UTIs

91
Q

Fosfomycin Pharmokinetics

A

40% oral bioavailability
t1/2 = 4 hours
Renally eliminated

92
Q

Fosfomycin ADRs

A

Diarrhea, vaginitis, nausea, headache

BIIC Cancers and Pharmo (10 decks)

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