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KN-Pharm Block 2 > Antimicrobials Reading > Flashcards

Antimicrobials Reading Flashcards

1
Q

What are 4 common mechanisms of antibacterial resistance?

A
  1. altering receptor targets
  2. decreased entry or efflux of drug out of microorganisms
  3. alterations in metabolic pathway
  4. inactivation of the drug
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2
Q

What are the 4 main targets of antibacterials?

A
  1. cell wall synthesis
  2. protein synthesis
  3. folic acid biosynthesis
  4. DNA/RNA synthesis
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3
Q

What is drug synergism?

A

When two drugs that have different mechanisms are used in conjunction to achieve amplified effects

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4
Q

How do penicillins work?

A

they inhibit cell wall synthesis by preventing formation of the peptidoglycan layer of the cell wall.

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5
Q

What do penicillins bind to?

A

transpeptidase enzyme, whose function is to cross-link N-acetyl muramic acid and N-acetyl glucosamine.
AND
they activate autolysins which destroy cell walls.
AND
carboxypeptidases and endopeptidases

There are several others and they are all referred to as penecillin-binding proteins (PBPs)

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6
Q

List the common PBPs.

A

transpeptidases, autolysins, carboxypeptidases, endopeptidases

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7
Q

How can bugs become resistant to penicillins?

A

modify their PBPs
actively pump the drug out of the cell
celave the B-lactam ring of penicillins with B-lactamases
alter their porins to prevent drugs from reaching PBPs

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8
Q

What will happen if penecillins are used in conjunction with bacteriostatics?

A

bacteriostatics halt cell growth. Penecillins rely on the cell growing and building cell wall to kill it. There will be a antagonistic interaction.

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9
Q

What type of drug is tetracycline?

A

it is a bacteriostatic which prevents cell growth and replication

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10
Q

What effect can penicillin have on oral contraceptives?

A

oral contraceptives rely on bacteria in the gut that cleave estrogen-glucoronide conjugates and allow for estrogenic reabsorption. These natural flora are often killed by penecillin, causing concern that the drug half-life may be decreased when on antibiotics

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11
Q

Can penicillin V be given orally? Penicillin G?

A

Yes. It is acid stable, unlike penicillin G, which is destroyed in the GI tract so can only be given IM

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12
Q

What are aminopenicillins?

A

Include ampicillin and amoxicillin. Synthetic penicillins that can be given enterally or parenterally.

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13
Q

What are penicillinase-resistant penicillins?

A

dicloxacillin, methicillin, oxacillin, nafcillin. They contain side groups that protect the drug from bacterial B-lactamases.

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14
Q

How is dicloxacillin usually given?

A

orally

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15
Q

How are methicillin, oxacillin, and nafcillin usually given?

A

parenterally.

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16
Q

What are antipseudomonal penicillins?

A

extended-spectrum penicillins. Inlcude carbenicillin, ticarcillin, mezlocillin and piperacillin. All except carbenicillin must be given parenterally.

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17
Q

What type of infections is oral carbenicillin useful for?

A

only reaches therapeutic levels in urinary tract

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18
Q

What are irreversible inhibitors of B-lactamases?

A

clavulanic acid, sulbactam, tazobactam. They inhibit B-lactamases to protect penicillins.

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19
Q

What are cephalosporins?

A

structurally resemble penicillin and possess B-lactam backbone, but are very stable to pH changes and can be taken with or without food.

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20
Q

If a patient reports they are allergic to penicillin is it ok to give them cephalosporins?

A

no. Cephalosporins are very similar to penicillin structurally and will likely cause an adverse reaction

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21
Q

What are carbapenems?

A

include imipenem, doripenem, ertapenem, and meropenem. Bactericidals that inhibit cell wall synthesis. B-lactam with a different structure so resistant to B-lactamases

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22
Q

What are telavancin and vancomycin?

A

interfere with cell wall by blocking polymerization and cross-linking of peptidoglycan by binding to the D-Ala-D-Ala portion of cell walls. Telavancin also disrupts membrane potential and changes cell permeability because of lipophilic side chain.

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23
Q

What is cycloserine?

A

inhibits cell wall synthesis in Gram- bacteria. Reserved for mycobacterium tuberculosis that is resistant to first-line antitubercular drugs

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24
Q

What is polymyxin B?

A

bactericidal for Gram- (except Proteus). It is a cationic detergent that disrupts lipoproteins in cell walls, thus increasing membrane permeability.

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25
Q

Which types of drugs interfere with bacterial protein synthesis?

A

aminoglycosides, macrolides, and tetracyclines

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26
Q

What are aminoglycosides?

A

amikacin, gentamicin, kanamycin, netilmicin, streptomycin, tobramycin, and neomycin. Bind to 30S ribosomal subunits to interfere with protein synthesis. Interfere with formation of initiation complex, misread mRNA and miscode AAs in growing peptides, and cause ribosomes to separate from mRNA, creating monosomes.

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27
Q

Can aminoglycosides be given orally?

A

no they are too water soluble. They are usually given parenterally. Penetrate the CNS and have short half-lives.

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28
Q

Where can aminoglycosides accumulate?

A

inner ear and renal cortex., causing nephro and oto-toxicity

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29
Q

What is the postantibiotic effect?

A

because aminoglycosides have a translational mechanism, microorganisms continue to die even after drug concentration declines.

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30
Q

Will aminoglycosides kill gram+ bacteria?

A

No, they are only effective for gram- bacterium

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31
Q

How can bacteria develop resistance to aminoglycosides?

A

they can alter receptor proteins on their ribosomes to prevent drug binding. They can also attack the aminoglycosides themsives with enzymes or other reactions. Resistance is especially common in anaerobes

32
Q

What are tetracyclines?

A

all drugs that end in -cycline. bacteriostatics. inhibit protein synthesis through reversible binding to bacterial 30S ribosomal subunits to prevent new incoming AAs, thus interfering with peptide growth.

33
Q

Which is the first line tetracycline used?

A

tigecycline

34
Q

What are the common modes of resistance to tetracyclines and which tetracycline can combat this?

A

efflux pumps and ribosomal protection.

glycylcycline can bypass these.

35
Q

How is doxycycline metabolized?

A

excreted in feces so safe for renal dysfunction patients

36
Q

How do gram+ bacteria become resistant to tetracyclines? Gram-?

A

efflux pumping.

Gram- prevent drug entry to membrane

37
Q

What is chloramphenicol?

A

bacteriostatic that binds to 50S ribosomal subunit and blocks linkage of incoming AAs by interfering with enzyme peptidyl transferase.

38
Q

How is chloramphenicol metabolized?

A

via glucoronidation. It accumulates in patients with hepatic disease, causing gray baby or gray adult, a syndrome in which people fail to eat, thrive, and become pale and cyanotic.

39
Q

What are Lincosamides?

A

clindamycin. interrupts protein synthesis by binding to 50S ribosomal subunits and preventing translocation of incoming AAs from ribosomal site A to site P.

40
Q

What are macrolides?

A

erythromycins and azithromycin. inhibit protein synthesis by binding to same site on prokaryotic ribosomal 50 S subunits as clindamycin and chloramphenicol. Prevent ranslocation of AAs from A site to P site. They can interefere with these other drugs and cause cross-resistance.
Can be either bacteriostatic or cidal

41
Q

How do bugs become resistant to macrolides?

A

they alter membrane permeability, methylate 50 S subunits to prevent binding, or enzymatically attack the drug.

42
Q

What are the adverse effects of erythromycins?

A

GI distress. Cholestatic hepatitis, which can potentiate the actions of other drugs by inhibiting P450 3A4 metabolism. Prolongs QT interval on EKGs.

43
Q

Which erythyromycin-like drug does not increase QT interval?

A

azithromycin

44
Q

What are ketolides?

A

telithromycin. Inhibits 50 S ribosomal subunits. Binds to two separate domains within the 50 S to decrease chance of resistance. It is also a poor substrate for efflux pumps making it even more powerful.

45
Q

What is retapamulin?

A

topical ointment pleuromutilin antibiotic that disrupts protein synthesis by interfereing with peptidyl transferase by binding to a unique site on 50S ribosomal subunit, and blocks P-site interactions

46
Q

What is mupirocon?

A

topical ointment antibiotic that inhibits tRNA that transports isoleucine. Causes no cross-resistances because the mechanism is different than all other antimicrobials.

47
Q

What is linezolid?

A

interferes with protein synthesis by binding to a unique site on the 50 S subunit, preventing formation of the 70 S complex.

48
Q

What are streptogramins?

A

combination of quinupristin and dalfopristin. acts at bacterial ribosomes and interferes with protein synthesis. Used to treat life-threatening infections by vancomycin-resistant enterococci and MRSA skin infections

49
Q

What is quinupristin?

A

a streptogramin that irreversibly blocks ribosomes and inhibits late phases of protein synthesis

50
Q

What is dalfopristin?

A

a streptogramin that inhibits early phases of protein synthesis.

51
Q

Describe the pathway of bacterial folic acid synthesis.

A

dihyrdopteridine and PABA converted to dihydropteroic acid by dihydropteroate synthetase. Dihydropteroic acid and glutamic acid form dihydrofolic acid.
Dihydrofolic acid converted to tetrahydrofolic acid by dihydrofolate reductase.

52
Q

What are sulfonamides?

A

compete with para-aminobenzoic acid at the first step of folic acid pathway

53
Q

What kind of drugs can sulfonamides interfere with?

A

sulfonamides are highly protein-bound and can displace other drugs that are protein-bound, such as warfarin. Can damage fetus in pregnant women because it displaces bilirubin.

54
Q

How does resistance to sulfonamides develop?

A

reduced bacterial uptake.
alternative metabolic pathways of folic acid
production of excessive para-aminobenzoic acid to compete with the drug.
altering dihydropteroate synthase to prevent drug binding

55
Q

How are sulfonamides metabolized?

A

hepatically, then renally excreted.

56
Q

What is trimethoprim?

A

inhibits dihydrofolate reductase, the enzyme that catalyzes the last step of bacterial folic acid synthesis.

57
Q

How does trimethoprim resistance develop?

A

reduced bacterial uptake
altered dihydrofolate reductase to prevent drug binding
overproduction of dihydrofolate reductase

58
Q

What are fluoroquinolones?

A

drugs ending in -floxacin. interefere with bacterial DNA synthesiss by inhibiting DNA gyrase or topoisomerase IV.

59
Q

What is DNA gyrase?

A

bacterial enzyme that is responsible for relaxing supercoiled DNA.

60
Q

What is topoisomerase IV?

A

enzyme involved in separating DNA into daughter cells during replication.

61
Q

Why is gemifloxacin special?

A

it inhibits both DNA gyrase and topoisomerase IV, making it hard to develop resistance to.

62
Q

What are lipopeptides?

A

daptomycin. binds to bacterial membrane, causing rapid epolarization of cell, halting DNA, RNA and protein synthesis, killing the ell.

63
Q

How is daptomycin metabolized?

A

excreted unchanged in urine

64
Q

What is metronidazole?

A

selectively absorbed by anaerobic bacteria and sensitive protozoa. It is reduced by reacting with ferrodoxin, causing production of toxic metabolites that inhibit DNA synthesis and degrade existing DNA, as well as nucleic acid synthesis, killing the cell.

65
Q

What is nitazoxanide?

A

intereferes with pyruvate/ferrodoxin oxidoreductase enzyme-dependent electron transfer, which is essential for anaerobic metabolism

66
Q

What is tinidazole?

A

causes cytotoxicity by damaging DNA and inhibiting synthesis.

67
Q

What are the downsides of metronidazoe, nitazoxanide, and tinidazole?

A

carcinogenic and cant be used during pregancy.

68
Q

What is rifaximin?

A

inhibits bacterial RNA synthesis by binding to DNA-dependent RNA polymerase

69
Q

How is rifaximin metabolized?

A

excreted unchanged in feces. Does not interfere with CYP450

70
Q

Why are mycobacteria hard to treat?

A

they grow slowly, can lie dormant, have thick impermeable cell walls, can reside within host cels, and quickly develop resistances.

71
Q

What is isoniazid?

A

inhibits synthesis of mycolic acids, essential components of mycobacterial cell walls.

72
Q

How is isoniazid metabolized?

A

acylation.

73
Q

What is rifampin?

A

inhibits bacterial RNA polymerase and prevents transcription. It is a potent inducer of drug metabolism and alters the plasma levels of many drugs

74
Q

What is pyrazinamide?

A

lowers pH in the tubercule cavity to inhibit growth of mycobacterium

75
Q

What is ethambutol?

A

inhibits RNA synthesis and decreases replication of tubercle bacilli

76
Q

What is clofazimine?

A

binds to mycobacterial DNA and inhibits RNA polymerase actions. Has very slow actions and require minimum of 2 years treatment, often for life.

KN-Pharm Block 2 (10 decks)

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