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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
What are the 4 antistaphylococcal Pencillins and what differentiates them from the other penicillins?
Beta-lactamase resistant used to treat B-lactamase producing staphylococci 1. Methicillin 2. Nafcillin 3. Oxacillin 4. Dicloxacillin
26
What are the extended spectrum Penicillins?
* Ampicillin * Amoxicillin
27
What are the clinical application of Amoxicillin?
* Acute otitis media * Streptococcal pharyngitis * PNA * Skin infections * **UTIs** Amoxicillin + Clavulanic Acid is prophylactic treatments for dog, cat, and human bites
28
What are the clinical applications of Ampicillin?
* Acute otitis media * Streptococcal pharyngitis * PNA * Skin infections * UTIs Ampicillin + Sulbactam for dog, cat, and human bites
29
What are the Antipseudomonal Penicillins and what differentates them?
* Carbenicillin * Ticarcillin * Piperacillin Effective against many _gram negative and gram positive bacilli_ **(P. aeruginosa)**
30
What are the clinical applications of antipseudomonal Penicillins?
* Pseudomonas auruginosa * Injectable treatment of Gram negative * Treatment of moderate-severe infections of suceptible organisms (skin, gynelogical, intra-abdominal, febrile neutropenia)
31
What are the pharmokinetic effects of distribution and excretion of Penicillins?
**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
What are 4 adverse effects of Penicillin?
* Hypersensitivity * GI disturbances * Pseudomembranous colitis (ampicillin) * Maculopapular rash (ampicillin, amoxicillin)
33
What is cephalosporins MOA and distinguishing feature from penicillin?
**MOA:** beta-lactam antibiotic same as penicillins Affected by similar resistance mechamisms but _less susceptible to beta-lactamases_
34
What are the generations of cephalosporins based on their classifications?
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
What are all cephalosporings inactive against?
**LAME** * **L**isteria * **A**typical (Chlamydia, Mycoplasma) * **M**RSA * **E**nterococci
36
What is the major mechanisms of cephalosporin resistance?
* Modification of target PBPs
37
What are the 1st generation cephalosporins and their clinical applications?
Cefazolin and Cephalexin * Rarely DOC for any infection * Cefazolin = DOC for surgical prophylaxis
38
What are the 2nd generation cephalosporins and their clinical applications?
Cefaclor, Cefoxitin, Cefotetan, Cefamandole * Sinusitis, otitis, and lower respiratory tract infections * Cefotetan & Cefoxitin = prophylaxis and therapy of abdominal/pelvic infections
39
What are the 3rd generation Cephalosporins and their clinical applications?
_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
What is the 4th generation cephalosporin and its clinical application?
Cefipime * Wide antibacterial spectrum * Treatment of mixed infection with susceptible organisms * Complication UTIs, complicatied intra-abdominal infections, febrile neutropenia
41
What is the pharmokinetic factors of cephalosporins?
* _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
What is the 5th generation cephalosporins and its clinical applications?
Ceftaroline * Activity against MRSA * Skin and soft tissue infection from MRSA, particulary if Gram-negative pathogens are co-infecting
43
What are the adverse effect of Cephalosporins?
* 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
What is the MOA of carbopenems and what differentiates them from penicillin?
**MOA:** synthetic beta-lactam antibiotics * Resist hydrolysis by most beta-lactamases
45
What are the carbapenems and their clinical applications?
Doripenem, Ertapenem, Imipenem, Meropenem * Use limited to life-threatening infecitons commonly extended spectrum beta-lactamase producing Gram-negatives
46
What the pharmokinetics of carbapenems?
* IV * _Imipenem forms nephrotoxic metabolite_ so but combine with _Cilastatin_ (dehydropeptidase I inhibitor)
47
What are the adverse effects of Carbapenems?
* Allergic reactions (partial cross-sensitivity with penicillin's) * GI distress * High levels of imipenem can cause CNS toxicity
48
What is the monobactam and was differentiates it from penicillin?
Aztreonam * Active against gram negative rods only (pseudomonas) * resistent to beta-lactamases
49
What are the clinical applications of Monobactram?
* Treatment of Gram-negative infections in patients allergic to penicillin
50
What are the adverse effects of Monobactam?
* Little cross-hypersensitivy with other beta-lactam antibiotics * Occasional skin rash and GI upset
51
What is the MOA, CA, AE of Vancomycin?
**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
What is the MOA of Daptomycin?
**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
What are the clinical applications of Daptomycin?
* treatment of severe infections caused by MRSA or VRE * treatment of complicated skin/structure infections cause by susceptible S. aureus
54
What is the pharmokinetics and adverse effects of daptomycin?
* Only given by IV * _Elevated creatine phosphokinases_ (so stop statins) * Constipation, nausea, headache, insomnia
55
What is the MOA, clinical application, and pharmokinetics of Bacitracin?
**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
What is the MOA, clinical applications, and pharmacokinetics of Fosfomycin?
**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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