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Pharm > Antibacterials - Cell Wall Synthesis Inhibitors > Flashcards

Antibacterials - Cell Wall Synthesis Inhibitors Flashcards

1
Q

Define bacteriostatic

A

reversible inhibition of growth

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2
Q

Define bactericidal

A

irreversible inhibition of growth

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3
Q

Define Minimal Inhibitory Concentration (MIC)

A

Lowest concentration of antibiotic that prevents visible growth

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4
Q

Define Minimal Bacterialcidial Concentration (MBC)

A

Lowest concentration of antibiotic that results in a 99.9% decline in colony count after overnight borth dilution incubations

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5
Q

What are the 6 considerations to select the right agent?

A
  1. Organism’s identity and susceptibility to an agent
  2. Necessity of empiric therapy
  3. Site of infection
  4. Pharmacology
  5. Patient factors
  6. Cost of therapy
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6
Q

What are the three major mechanisms of antibiotic resistance?

A
  1. Altered uptake of antibiotic
  2. Altered target
  3. Drug inactivation
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7
Q

What is the difference between primary resistance and aquired drug resistance?

A
  • Primary resistance - structural absence of target for drug to act on
  • Acquired resistance - spontaneous mutation of DNA, DNA transfer, or altered expression of proteins in drug-resistant organisms
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8
Q

Transfer of genetic information can occur due to?

A
  1. Conjugation (F+ plasmid for sex pilus)
  2. Transposons (mobile genetic elements)
  3. Transduction (bacteriophage)
  4. Transformation (DNA uptake)
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9
Q

What are 3 complications of antibiotic therapy?

A
  1. Hypersensitivity
  2. Direct toxicity
  3. Superinfection
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10
Q

What are the 4 MOA for antibacterials?

A
  • Cell wall synthesis inhibitors
  • Protein synthesis inhibitors
  • Drugs that affect nucleic acid synthesis
  • Miscellaneous and urinary antiseptics
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11
Q

What are the mechanisms of synergism?

A
  • Sequential blockade
  • Blockade of drug-inactivating enzymes
  • Enhanced drug uptake
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12
Q

What are the cell wall synthesis inhibitors?

A
  • B-lactam (penicillins, cephalosporins, carbapenems, monobactams)
  • Vancomycin
  • Daptomycin
  • Bacitracin
  • Fosfomycin
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13
Q

Beta-lactams MOA?

A

MOA: bactericidal that inhibits the last step in peptidoglycan synthesis by binding to PBPs and activate autolytic enzymes to initiate cell death

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14
Q

What is the mechanism of Beta-Lactamases?

A

bacterial enzymes (pinicillinases, cephalosporinases) that hydrolyze the Beta-lactam ring to inactivate it

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15
Q

What are the 3 beta-lactamase inhibitors and what is their MOA?

A
  1. Clavulanic Acid
  2. Sulbactam
  3. Tazobactam

MOA: have beta-lactam ring with no antibacterial activity that will bind and inactivate beta-lactamses

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16
Q

What determines penicillins ability to reach PBPs?

A
  • Size
  • Charge
  • Hydrophobicity
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17
Q

What is the antibacterial spectrum for penicillins and why?

A
  • Gram-positive: cell wall easily crossed
  • Gram-negative: porins to permit transmembrane entry
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18
Q

What is a synergistic combination for penicillin and why?

A

Penicillin + Aminoglycoside: penicillin facilitate movement of aminoglycosides through cell wall, need different infusions because will form inactive complex, and is an effective emperic treatment for infective endocarditis

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19
Q

What are the 4 general mechanisms of penicilin resistance?

A
  1. Inactivation by B-lactamase
  2. Modification of target PBPs
  3. Impaired penetration of drug to target PBPs
  4. Increased efflux
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20
Q

What are the clinical applications Penicillin G?

A
  • Mostly used for Gram + organisms
  • Syphilis (benzathine penicillin G)
  • Strep Infections
  • Susceptible pneumococci
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21
Q

What are the 2 repository penicillins and what are their purpose?

A
  • Penicillin G Procaine (12-24hr) and Penicillin G Benzathine (3-4wks)
  • Developed to prolong during of Penicillin G
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22
Q

What are the clinical application of Penicillin G Benzathine?

A
  • syphilis
  • Rheumatic fever prophylaxis
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23
Q

What is the importance that differentiates Penicillin V?

A

More acide stable that G so can be given orally

24
Q

What is the clinical application of Penicillin V?

A

Mild to moderate:

  • Pharyngitis
  • Tonsilitis
  • Skin infections (caused by Strep)
25
Q

What are the 4 antistaphylococcal Pencillins and what differentiates them from the other penicillins?

A

Beta-lactamase resistant used to treat B-lactamase producing staphylococci

  1. Methicillin
  2. Nafcillin
  3. Oxacillin
  4. Dicloxacillin
26
Q

What are the extended spectrum Penicillins?

A
  • Ampicillin
  • Amoxicillin
27
Q

What are the clinical application of Amoxicillin?

A
  • Acute otitis media
  • Streptococcal pharyngitis
  • PNA
  • Skin infections
  • UTIs

Amoxicillin + Clavulanic Acid is prophylactic treatments for dog, cat, and human bites

28
Q

What are the clinical applications of Ampicillin?

A
  • Acute otitis media
  • Streptococcal pharyngitis
  • PNA
  • Skin infections
  • UTIs

Ampicillin + Sulbactam for dog, cat, and human bites

29
Q

What are the Antipseudomonal Penicillins and what differentates them?

A
  • Carbenicillin
  • Ticarcillin
  • Piperacillin

Effective against many gram negative and gram positive bacilli (P. aeruginosa)

30
Q

What are the clinical applications of antipseudomonal Penicillins?

A
  • Pseudomonas auruginosa
  • Injectable treatment of Gram negative
  • Treatment of moderate-severe infections of suceptible organisms (skin, gynelogical, intra-abdominal, febrile neutropenia)
31
Q

What are the pharmokinetic effects of distribution and excretion of Penicillins?

A

Distribution: therapeutic levels in pleural, pericardial, peritoneal, synovial fluids, urine, and CSF (meningitis) but insufficient in prostate and eye

Excretion: primarily via kidney except for Naficillin is primarily excreted in bile

32
Q

What are 4 adverse effects of Penicillin?

A
  • Hypersensitivity
  • GI disturbances
  • Pseudomembranous colitis (ampicillin)
  • Maculopapular rash (ampicillin, amoxicillin)
33
Q

What is cephalosporins MOA and distinguishing feature from penicillin?

A

MOA: beta-lactam antibiotic same as penicillins

Affected by similar resistance mechamisms but less susceptible to beta-lactamases

34
Q

What are the generations of cephalosporins based on their classifications?

A

Based on:

  • Order of introduction into clinical use
  • Spectrum of activity

1-3rd: Gram positive activity diminished while Gram negative activity increased from first to third

4th: Gram positive cocci and Gram negative bacilli

5th: similar to thirds with activity against MRSA

35
Q

What are all cephalosporings inactive against?

A

LAME

  • Listeria
  • Atypical (Chlamydia, Mycoplasma)
  • MRSA
  • Enterococci
36
Q

What is the major mechanisms of cephalosporin resistance?

A
  • Modification of target PBPs
37
Q

What are the 1st generation cephalosporins and their clinical applications?

A

Cefazolin and Cephalexin

  • Rarely DOC for any infection
  • Cefazolin = DOC for surgical prophylaxis
38
Q

What are the 2nd generation cephalosporins and their clinical applications?

A

Cefaclor, Cefoxitin, Cefotetan, Cefamandole

  • Sinusitis, otitis, and lower respiratory tract infections
  • Cefotetan & Cefoxitin = prophylaxis and therapy of abdominal/pelvic infections
39
Q

What are the 3rd generation Cephalosporins and their clinical applications?

A

Ceftiaxone, Cefoperazone, Cefotaxime, Ceftazidime, Cefixime

  • Highly active against enterobacteriacae, Neisseria, and H. influenzae
  • DOC for gonorrhea (Ceftriaxone)
  • DOC for empiric treatment of meningitis (Ceftriaxone
  • Prophylaxis of meningitis (Ceftriaxone)
  • Treatment of disseminated Lyme disease (Ceftriaxone)
  • Activity against P. aeruginosa (Cefoperazone and Ceftazidime)
40
Q

What is the 4th generation cephalosporin and its clinical application?

A

Cefipime

  • Wide antibacterial spectrum
  • Treatment of mixed infection with susceptible organisms
  • Complication UTIs, complicatied intra-abdominal infections, febrile neutropenia
41
Q

What is the pharmokinetic factors of cephalosporins?

A
  • Most administered paraenterally (exceptions = cephalexin, cefaclor, cefixime)
  • Only 3rd generation reach adequate levels in CSF
  • Mainly eliminated by kidneys (exceptions = ceftriaxone & cefoperazone excreted in bile)
42
Q

What is the 5th generation cephalosporins and its clinical applications?

A

Ceftaroline

  • Activity against MRSA
  • Skin and soft tissue infection from MRSA, particulary if Gram-negative pathogens are co-infecting
43
Q

What are the adverse effect of Cephalosporins?

A
  • Allergic reactions (minor penicillin allergic pts treated with cephalosporin)
  • Superinfection from C. difficile
  • Cefamandole, cefoperazone, and cefotetan have methyl-thiotetrazole group that can cause:
    • Hypoprothrombinemia
    • Disulfiram-like reactions
44
Q

What is the MOA of carbopenems and what differentiates them from penicillin?

A

MOA: synthetic beta-lactam antibiotics

  • Resist hydrolysis by most beta-lactamases
45
Q

What are the carbapenems and their clinical applications?

A

Doripenem, Ertapenem, Imipenem, Meropenem

  • Use limited to life-threatening infecitons commonly extended spectrum beta-lactamase producing Gram-negatives
46
Q

What the pharmokinetics of carbapenems?

A
  • IV
  • Imipenem forms nephrotoxic metabolite so but combine with Cilastatin (dehydropeptidase I inhibitor)
47
Q

What are the adverse effects of Carbapenems?

A
  • Allergic reactions (partial cross-sensitivity with penicillin’s)
  • GI distress
  • High levels of imipenem can cause CNS toxicity
48
Q

What is the monobactam and was differentiates it from penicillin?

A

Aztreonam

  • Active against gram negative rods only (pseudomonas)
  • resistent to beta-lactamases
49
Q

What are the clinical applications of Monobactram?

A
  • Treatment of Gram-negative infections in patients allergic to penicillin
50
Q

What are the adverse effects of Monobactam?

A
  • Little cross-hypersensitivy with other beta-lactam antibiotics
  • Occasional skin rash and GI upset
51
Q

What is the MOA, CA, AE of Vancomycin?

A

MOA: bacterial glycoprotein the binds D-Ala-D-Ala terminus of nascent peptidoglycan pentapeptide to inhibit bacterial cell wall synthesis

CA: serious infections caused by B-lactam resistent Gram positive organisms (MRSA) and gram positive infections in patients severly allergic to B-lactams

PK: requires slow IV, renal excretion

AE: Red man/neck syndrome, ototoxicity, nephrotoxicity

52
Q

What is the MOA of Daptomycin?

A

MOA: binds cell membrane via calcium-dependednt insertion of lipid tail > depolarization of cell membrane with K+ efflux > cell death

  • Novel mechanism of action useful against multi-drug resistant bacteria
53
Q

What are the clinical applications of Daptomycin?

A
  • treatment of severe infections caused by MRSA or VRE
  • treatment of complicated skin/structure infections cause by susceptible S. aureus
54
Q

What is the pharmokinetics and adverse effects of daptomycin?

A
  • Only given by IV
  • Elevated creatine phosphokinases (so stop statins)
  • Constipation, nausea, headache, insomnia
55
Q

What is the MOA, clinical application, and pharmokinetics of Bacitracin?

A

MOA: interferes in late stage wall synthesis in unique mechanisms so no cross resistance

  • Effective against Gram positive organisms
  • Marked nephrotoxicit to mainly topical use
56
Q

What is the MOA, clinical applications, and pharmacokinetics of Fosfomycin?

A

MOA: inhibits cytoplasmic enzyme enolpyruvate transferase in early stage cell wall synthesis

  • Treatment of uncomplicated lower UTI’s
  • Given orally

Pharm (14 decks)

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