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Pharmacology > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

4 mechanisms of antibacterial resistance

A

alteration in receptor target, decreased entry/efflux, alteration in metabolic pathway, inactivate drug

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2
Q

Penicillin mechanism of action

A

bind PBP (transpeptidase that cross links NAG and NAM, autolysins, endopeptidase, carboxypeptidase)

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3
Q

4 mechanisms of antebacterial resistance to penicillin

A

modification of PBP, active pumping out of drug, cleave B lactam ring, altered porins in gram negative bacteria.

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4
Q

When penicillins are combined with drugs that are _____, pharmacologic antagonism results.

A

bacteriostatic

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5
Q

With oral contraceptives, gut bacterial normally cleave _____ conjugates, allowing estrogen to be reabsorbed and recycled via the ______ pathway.

A

estrogen-glucuronide conjugates, enterohepatic recirculation

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6
Q

Which types of penicillins are given for gram positive bacteria?

A

natural penicillins, penicillinase resistant penicillins

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7
Q

Which types of penicillins are given for gram negative bacteria?

A

amino, anti-pseudomonal

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8
Q

What are the common natural penicillin drugs?

A

Penicillin G and penicillin V

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9
Q

How is penicillin G administered?

A

intravenously or intramuscularly–> it is readily destroyed in acidic environments

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10
Q

How is penicillin V administered?

A

it is more stable than penicillin G so it is administered orally, but on empty stomach

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11
Q

What are the common aminopenicillins?

A

amoxicillin, ampicillin

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12
Q

How is ampicillin administered?

A

enterally or parenterall, oral must be on empty stomach

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13
Q

How is amoxicillin administered?

A

orally, with or without food because it is more stable

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14
Q

Rate penicillin G, V, amoxicillin, and ampicillin based on stability in an acidic enviornment.

A

Pen G, ampicillin and V, amoxicillin

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15
Q

What are the common penicillinase-resistant penicillins?

A

dicloxacillin, oxicillin, methicillin, naficillin

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16
Q

Mechanism of action of penicillinase resistant penicillins

A

they contain side groups that protect them from being inactivated by B-lactamases

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17
Q

Which penicillinase resistant penicillin is given orally?

A

dicloxacillin

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18
Q

What are the common anti-pseudomonal penicillins?

A

carbenicillin, ticarcillin, piperacellin, mezlocillin

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19
Q

Which antipseudomonal penicillin is given orally?

A

carbenicillin

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20
Q

Where are the therapeutic levels of carbenicillin found and what does this imply?

A

urinary tract: limits utility to UTI and prostate infections

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21
Q

What are the common irreversible inhibitors or B lactamases?

A

clavulanic acid, sulfbactam, tazobactam

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22
Q

Cephalosporins structurally resemble _____. Why?

A

penicillins, they have a B lactam back bone

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23
Q

What penicillin might be given to treat a prostate infection?

A

carbenicillin

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24
Q

Adverse effects of cephalosporins

A
  1. cross reactivity with penicillin allergy
  2. GI irratiation, take with food
  3. disruption of normal flora may cause secondary infections
  4. renal toxicity
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25
Q

What pre-existing disease indicates need for caution when administering cephalosporin?

A

renal disease

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26
Q

Common carbapenem drugs

A

dorypenem, imipenem/cilastatin, ertapenem, meropenem

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27
Q

MAO of carbapenems

A

bacteriocidal, inhibit cell wall synthesis, different B lactam ring, so resistant to B lactamases

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28
Q

MAO of telavancin, vancomycin

A

Inhibit cell wall synthesis by binding D-Ala D-Ala portion of cell walls. Telavancin disrupts membrane potential and changes in permeability due to lipophilic side chain moiety

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29
Q

MAO of cycloserine

A

inhibits cell wall synthesis in gram positive, negative but reserved for resistant TB

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30
Q

MAO of polymyxin B

A

bacteriocidal to all gram - bacilli (not Proteus). Cationic detergent that disrupts lipoproteins in cell walls thus increasing permeability

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31
Q

Common aminoglycosides

A

streptomycin, tobramycin, amikamicin, neomycin, kanamycin, netilmicin

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32
Q

Aminoglycosides bind to the ____ ribosomal subunit.

A

30S

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33
Q

4 ways aminoglycosides interfere with protein synthesis

A

formation on initiation complex, misread RNA, ribosomes separate from mRNA. formation of monosome

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34
Q

How are aminoglycosides administered?

A

parnterally. they are highly polar cations so they are too water soluble

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35
Q

PK of aminoglycosides

A

short half live, ototoxic, nephrotoxic, postantibiotic effect

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36
Q

Are aminoglycosides used for gram neg or pos?

A

negative

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37
Q

Tetracycline drugs

A

tetracyclines, doxycycline, demecycline, oxytetracyline, tigecycline

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38
Q

Tetracyclin MOA

A

Binds 30S preventing binding of aminoacyl-tRNA, interfere with peptide growth. Bacteriostatic against G- and G+

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39
Q

What are glycylcycline?

A

antibiotics derived from tetracycline that are designed to overcome two common mechanisms of tetracycline resistance (efflux pumps and ribosomal protection). Tigecycline

40
Q

Of all the tetracycline derivatives, _____ is most closely related to minocycline.

A

tigecycline

41
Q

Mode of penetrance in tetracycline

A

G-: passive, G+: active

42
Q

Tetracycline PK

A

gastric absorption is inhibited by chelation due to divalent cations or bile acid resins. Best to administer on empty stomach

43
Q

Which tetracycline is the safest option for patients with renal dysfunction?

A

Doxycycline: metabolized hepatically, excreted in feces

44
Q

Tetracycline resistance

A

G+: acquire resistance to tetracyclines by actively pumping out via. G-: alterations in outer membrane proteins

45
Q

Chloramphenicol MOA

A

Bacteriostatic, binds 50S, blocks incoming amino acids, interferes with peptidyl transferase

46
Q

How is chloarmphenicol metabolized?

A

via glucuronidation

47
Q

What are dangers of giving chloramphenicol to someone with hepatic disease?

A

ineffiecient glucuronidations resulting in gray baby

48
Q

Lincosamide drug

A

clindamycin

49
Q

MOA lincosamide

A

binds 50S, prevents translocation from A to P site

50
Q

Macrolide drug

A

erythromycin base, estolate, stearate, ethylsuccinate, clarithromycin, axithromycin

51
Q

Macrolide MOA

A

inhibit protein synthesis by binding to 50S–> prevent translocation from A to P site, can be bacteriocidal or static depending on concentration

52
Q

What cross-resistance can occur with macrolides?

A

because it shares the same binding site with clindamyin and chloramphenicol, they can interfere with each other and cause cross resistance

53
Q

How can microorganisms become resistant to macrolides?

A

altered permeability, methylate 50S, develope enzymatic mechanisms to destroy the drugs

54
Q

Erythromycin adverse effects

A

GI distress, cholestatic hepatitis (estolate salt), inhibiting P450 3A4 can cause toxicity, prolong QT interval–> torsades do pointes

55
Q

Clarithromycin adverse effects

A

prolongs QT interval, inhibits P450 3A4, but less GI distress than erythromycin

56
Q

Azithromycin adverse effects

A

does NOT prolong QT interval or inhibit P450 3A4,

57
Q

Ketolide drugs

A

Telithromycin

58
Q

MOA ketolides

A

inhibits 50S by binding 2 separate subunits. This means that 2 mutations would be needed to develop resistance. Poor substrate for efflux.

59
Q

Retapamulin drug

A

ointment, pleuromutilin

60
Q

Retapamulin MOA

A

interferes with peptidyl transferase by binding to unique spot on 50S.

61
Q

Mupirocin MOA

A

topical cream and ointment that inhibits tRNA with ile

62
Q

___ has no cross resistance with any other antimicrobial.

A

Mupirocin

63
Q

Linezolid

A

interferes with protein synthesis by binding to 50S that prevents formation of the functional 80S complex

64
Q

Streptogramins drugs

A

quinipristin and dalfopristin

65
Q

Streptogramins MOA

A

acts at bacterial ribosomes and intereferes with protein synthesis. Quinupristin blocks late in protein synthesis, dalfopristin inhibits early.

66
Q

When are streptogramins used?

A

treat life threatening infections caused by vancomycin resistant enterococci and skin infections caused by MRSA

67
Q

Sulfanoamide drugs

A

sulfadiazine, silver sulfadiozine, sulfisoxazole, sulfmethoxazole, sulfacetamide, sulfasalazine

68
Q

Sulfonamide MOA

A

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

69
Q

What can cause adverse effects with sulfanoamides?

A
  1. highly protein bound, can displace other drugs like warfarin.
  2. Displaces bilirubin: bad in pregnant women and infants younger than 2 months. Hyperbilirubinemia can cause kerincterus
70
Q

How does bacteria develop resistant to sulfanoamides?

A

reduced uptake of drugs, alternate metabolic pathways, production of excess para-aminobenzoic acid, alterations in dihyropteroate synthase

71
Q

how are sulfanoamides metabolized?

A

hepatically via acetylation, oxidation, glucuronidation–> slow acetylators may be at risk for hypersensitivity reaction . excreted renally

72
Q

Trimethoprim MOA

A

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

73
Q

How can bacteria develop resistance to trimethoprim?

A

reduced uptake, alterations in dihydrofolate reductase, overproduction of dihydrofolate reductase

74
Q

Fluoroquinolone drugs

A

besi-, cipro-, gati-, gemi-, levo-, moxi-, nor-, of- floxacin

75
Q

MOA fluorquinolones

A

bacteriocidal. inhibit gyrase or topioisomerase IV.

76
Q

Why is it hard for bacteria to develop resistance to gemifloxacin?

A

inhibits both gyrase and topioisomerase IV

77
Q

What affects absorption of fluorquinolones?

A

food/cations: calcium, iron, aluminum, magnesium, zinc, sucralfate

78
Q

Distribution of fluoquinolones

A

minimal to CNS, all other compartments

79
Q

Lipopeptide drug

A

daptomycin

80
Q

lipopeptide MOA

A

daptomycin binds bacteria membrane–> depolarization–> RNA, DNA, protein synthesis stopped –> cell death

81
Q

how is daptomycin excreted?

A

unchanged in the urine

82
Q

Metronidazole MOA

A

absorbed by anerobic bacteria and sensitive protazoa, reduced by ferrdoxin (generated by pyruvate/ferredoxin oxido-reductase–> toxic metabolites–> inhibition of DNA synthesis, degradation of DNA, etc.. death…mutagenic/carcinogenic. Not given in first trimester

83
Q

nitazoxanide moa

A

interferes with pyruvate/ferredoxin oxido-reductase enzyme dependent electron transfer essential for anaerobic metabolism…carcinogenic/mutagenic. Not given in first trimester

84
Q

Tinidazole moa

A

cytotoxicity via damage to DNA and inhibiting DNA synthesis

85
Q

How is metronidazole used?

A

penetrates the CNS so it can be used to treat meningitis and brain abscesses caused by anerobes.

86
Q

Rifaximim MOA

A

rifampin derivative that inhibits bacterial RNA synthesis by binding to bacterial DNA dependent RNA polymerase

87
Q

Rifaximin PK

A

drug excreted unchanged in feces, does not interfere with p450

88
Q

Isoniazid MOA

A

inhibits synthesis of mycolic acids

89
Q

Isoniazid distribution

A

total body water including CNS

90
Q

Metabolism of isoniazid

A

acetylation

91
Q

Rifampin MOA

A

inhibits bacterial RNA polymerase by suprressing initation of RNA chain formation

92
Q

Why are drug-drug interactions a major concern for rifampin?

A

it is a potent inducer of drug metabolism and alters the levels of many drugs

93
Q

pyrazinamide MOA

A

unclear–> lowers pH and inhibit growth?

94
Q

Ethambutol MOA

A

inhibits RNA synthesis and decreases replication of tubercle bacillia

95
Q

Clofazimine MOA

A

binds mycobacterial DNA and inhibits RNA polymerase actions. Slow acting

96
Q

treatment options of mycobacterial infections

A

isoniazid, rifampin, pyrazinamide, ethambutol, clofazimine

Pharmacology (4 decks)

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