antibiotics MT1 Flashcards

1
Q

what are the 5 different ways that antibiotics work (mechanisms of action)

A
  1. inhibition of cell wall synthesis
  2. inhibition of protein synthesis
  3. inhibition of nucleic acid synthesis
  4. alteration of cell membrane function
  5. alteration of cell metabolism
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2
Q

a microbiology lab determines the _______ by mixing a standard concentration of the organisms that the patient has grown with increasing concentrations of the antibiotic in a broth solution. the mixture with the lowest concentration of antibiotic where there is no visible growth is deemed to be the ___________

A

MIC - minimun inhibitory concentration

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3
Q

is this susceptible, intermediate or resistant?
if the MIC < breakpoint, at typical doses the antibiotic would have a high probability of being effective

A

susceptible (S)

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4
Q

is this susceptible, intermediate or resistant?
if the MIC is approaching or near the determined breakpoint. the antibiotic may be effective at higher doses (if safely attainable)

A

intermediate (I)

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5
Q

is this susceptible, intermediate or resistant?
if the MIC is greater than the breakpoint the antibiotic would be unlikely to achieve therapeutic success

A

resistant (R)

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6
Q

what three classes of antibiotics are bacteriostatic?

A
  • macrolides (azithromycin, clarithromycin, erythromycin)
  • tetracyclines (doxycycline)
  • linezolid
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7
Q

what are some mechanisms of resistance that bacteria can produce

A
  • enzymatic destruction
  • altered binding sites
  • efflux pumps
  • modified cell wall porins
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8
Q

what antibiotics are considered to be beta-lactams

A

penicillins (e.g. pen V/G, amoxicillin, cloxacillin)
cephalosporins (cephalexin, cefuroxime, cefixime)
carbapenems (imipenem, meropenem, ertapenem)

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9
Q

what are some examples of macrolides

A

erythromycin, clarithromycin, azithromycin

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10
Q

what are some examples of tetracyclines

A

tetracycline, doxycycline, minocycline

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11
Q

what are some examples of fluoroquinolones

A

ciprofloxacin, norfloxacin, levofloxacin, moxifloxacin

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12
Q

what are some examples of aminoglycosides

A

gentamicin and tobramycin

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13
Q

what is the mechanism of action of beta-lactams

A

beta-lactams bind to penicillin binding proteins (PBP) which cause the peptidoglycan barrier to not form properly causing cell lysis.

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14
Q

what is the most common mechanism of bacterial resistance in beta-lactams

A

enzymatic destruction and altered PBP sites

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15
Q

are beta-lactams bactericidal or bacteriostatic

A

bactericidal

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16
Q

are beta-lactams time dependant or concentration dependant

A

time dependant

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17
Q

what is the most common ADR for beta-lactams

A

hypersensitivity reaction

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18
Q

true/false: delayed rashes caused by penicillin, if after a few doses/days and NO itchiness/hives are typically indicative of a true IgE-mediated allergy

A

false - worried if rash happens right away with itchiness/hives

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19
Q

what should be done when patients have an uncertain penicillin allergy (such as reaction took place >10 years ago, or when reaction took places after days rather than hours when taking the antibiotic

A

refer patients for skin testing

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20
Q

if patient develops a rash with no itching/urticaria from penicillin, what other drug can be given?

A

a beta-lactam such as a cephalosporin can be given

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21
Q

this cephalosporin has a unique side chain to all other beta-lactams

A

cefalozolin

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22
Q

this beta-lactam is known for causing idiopathic skin rashes (maculopapular - not allergy associated)

A

amoxicillin

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23
Q

this beta-lactam seems to cause more hematologic issues

A

pip-tazo

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24
Q

this beta-lactam can bind to Ca (causing precipitation) and biliary slugging, mostly in paediatrics therefore should not use together with IV Ca

A

Ceftriaxone

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25
Q

this beta-lactam can cause seizure in renal dysfunction

A

cefepime

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26
Q

what pencillins must be taken on an empty stomach

A

Pen V and cloxacillin

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27
Q

all of the oral cephalosporins have excellent oral absorption except these two

A

cefixime and cefuroxime

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28
Q

this type of bacteria produces beta-lactamases, therefore the primary pencillins (pen V and pen G) did not have coverage for them. Cloxacillin was then introduced to help cover this type of bacteria

A

staph aureus

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29
Q

true/false: cloxacillin has strep coverage

A

true - not DOC but cloxacillin is active against strep spp.

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30
Q

these bind to beta-lactamase enzymes and therefore restore any susceptibility that was lost due to bacterial development of beta-lactamases (e.g. staph aureus, h. influenza, moxarella) and bacteria that always intrinsically produced beta-lactamases (e.g. b. frag)

A

beta-lactamase inhibitors (e.g. clavulin, tazobactam)

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31
Q

this penicillin medication was introduced to help cover gram -ve bacteria. it has a longer side chain which allows it to bind to different sites (PBP) and therefore has better gram negative coverage including some Pseudomonas spp.

A

piperacillin/tazobactam

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32
Q

true/false: as you go up in generations of cephalosporins, you get more gram -ve coverage

A

true

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33
Q

what are examples of first generation cephalosporins

A

cefadroxil, cephalexin, cefazolin
“CEFA”

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34
Q

what pneumonic can be used to remember the gram -ve coverage for first gen cephalosporins

A

PEK
P-proteus spp.
E- e.coli (not ESBLs)
K-Klebsiella (not ESBLs)

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35
Q

what are some examples of second generation cephalosporins

A

cefuroxime, cefprozil, cefoxitin

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36
Q

what pneumonic can be used to remember the gram -ve coverage for second gen cephalosporins

A

HPEK
H- H.influenzae (and M. catarrhalis)
P-proteus spp.
E- e.coli (not ESBLs)
K-Klebsiella (not ESBLs)

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37
Q

what are examples of third generation cephalosporins

A

cefixime, cefotaxime, ceftriaxone, ceftazidime
“ends in one or me”

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38
Q

what pneumonic can be used to remember the gram -ve coverage for third gen cephalosporins

A

HENPEK
H - H.influenzae
E- enterobacter spp.
N- N. meningiditis
P-proteus spp.
E- e.coli (not ESBLs)
K-Klebsiella (not ESBLs)

39
Q

this third generation cephalosporin has very poor activity against gram positive bacteria.

A

cefatazidime

40
Q

What are some examples of fourth generation cephalosporins

A

Ceftobiprole and cefepime

41
Q

What are examples of fifth generation cephalosporins

A

Ceftolozone/tazobactam

42
Q

If you over treat with this second generation cephalosporin, it will cause an influx of beta-lactamases

A

Cefoxitin (IV)

43
Q

these are structurally more resistant to beta-lactamases. has a major toxicity of seizures.

A

Carbapenems (e.g. imipenem, meropenem, ertapenem)

44
Q

true/false: all carbapenems are DOC for e.coli, klebsiella (non-ESBLs) and B.frag

A

false - covers ESBLS!!

45
Q

what is the MOA for macrolides

A

bind to the 50S subunit and inhibits protein synthesis

46
Q

what is the MOR for macrolides

A

europe - alteration of ribosomal binding site
North America - reduced permeability of cell membrane/reflux

47
Q

true or false: macrolides have a prolonged antibiotic effect (PAE)

A

true

48
Q

are macrolides time or concentration dependant

A

time (azithromycin is conc. dependant DAAMQ)

49
Q

are macrolides bacteriostatic or cidal

A

bacteriostatic

50
Q

this macrolide should be taken on an empty stomach

A

erythromycin

51
Q

what are some ADRs of macrolides

A
  • taste disturbances
  • Qt prolongation
52
Q

this tetracycline is similar to erythromycin and Pen G/V in that it is the first tetracycline and therefore has the least antimicrobial spectra of the tetracyclines.

A

tetracycline

53
Q

what is the MOA of tetracyclines

A

binds to 30S ribosomal subunit therefore inhibits protein synthesis

54
Q

what is the MOR for tetracyclines

A

decreased intracellular accumulation due to efflux by bacteria protein pump

55
Q

are tetracyclines bacteriostatic or cidal

A

static (in MTL)

56
Q

are tetracyclines time dependant or concentration dependant

A

time dependant

57
Q

true or false: tetracyclines have prolonged antibiotic effects

A

true

58
Q

which tetracycline should be taken on an empty stomach

A

tetracycline

59
Q

what are the most common ADRs for tetracyclines

A
  • photosensitivity
  • avoid with divalent cations
  • esophageal ulceration
  • baby teeth may turn gray
60
Q

__________ is LEAST likely to cause C. diff infection

A

tetracyclines

61
Q

this class of antibiotics are the opposite of the beta-lactams in that they started out with great gram -ve coverage but not great gram +ve.

A

fluorquinolones

62
Q

what is the MOA of fluoroquinolones

A

DNA! blocks bacterial DNA synthesis by inhibiting bacterial topoisomerase II (DNA gyrase and IV

63
Q

what is the MOR of fluoroquinolones

A

alterations in DNA gyrase making it difficult for a fluoroquinolone to bind

64
Q

are fluoroquinolones bacteriostatic or cidal

A

cidal

65
Q

are fluoroquinolones concentration or time dependant

A

concentration

66
Q

what fluoroquinolones need to be really adjusted

A

levo and cipro NOT MOXI

67
Q

what are ADRs in fluoroquinolones

A
  • can affect sugars
  • QT prolongation
  • photosensitivity
  • drowsiness
  • confusion
  • tendinopathy
68
Q

what are examples of ahminoglycosides

A

gentamicin and tobramycin

69
Q

what is the MOA of ahminoglycosides

A

binds to 30S ribosomal subunit and results in a defective cell membrane

70
Q

true or false: ahminoglycosides have a significant post-antibiotic effect (PAE)

A

true

71
Q

what are some ADRs of aminoglycosides

A
  • nephrotoxicity
  • ototoxicity
  • neuromuscular blockade
72
Q

true or false: aminoglycosides only cover gram +ve bacteria

A

false - only gram negative

73
Q

what is the MOA of vancomycin?

A

inhibits cell wall synthesis and the cell membrane is also damaged

74
Q

true or false: vancomycin is used IV to treat C. diff

A

false - used po to treat C diff as it stays in the GI tract and stays in contact with the C.diff

75
Q

what is the MOR for vancomycin

A

it binds to the extra peptidoglycan layers which are dead binding sites and therefore cannot reach the site of action

76
Q

true or false: vancomycin essentially only covers gram +ve

A

true

77
Q

true or false: vancomycin should only be used when a bacteria is resistant to other antibiotics or other antibiotics cannot be used due to ADRs or allergies

A

true

78
Q

what are some ADRs of vancomycin

A
  • infusion reactions
  • otoxicity
  • nephrotoxicity
79
Q

what is the MOA of clindamycin

A

binds to the 50S ribosomal subunit, inhibiting protein synthesis

80
Q

what is the MOR of clindamycin

A
  • mutation of the ribosomal receptor site
  • modification of the receptor
  • enzymatic inactivation of clindamycin
81
Q

is clindamycin bacteriostatic or cidal

A

static

82
Q

what is one main ADR of clindamycin

A

diarrhea!! probably the worst for causing C. diff

83
Q

this inhibits bacteria synthesis of dihrdyofolic acid by competition with para-amino benzoic acid

A

sulfamethoxazole

84
Q

this blocks the production of THF acid from dihyrofolic acid by reversibility inhibiting the requires enzyme dihydrofolate reductase

A

trimethoprim

85
Q

is TMP-SMX bacteriostatic or cidal

A

each are static on their own but cidal together

86
Q

is TMP-SMX concentration or time dependant

A

time

87
Q

what are some ADRs of TMP-SMX

A
  • SJS/TEN
    -avoid in pregnancy
    N/V/D
88
Q

this medication has an MOA of altering bacterial ribosomal proteins which inhibits synthesis of DNA, RNA and proteins

A

nitrofurantoin

89
Q

this medication is exclusively used for UTIs and should not be used if a CrCl of < 30 ml/min

A

nitrofurantoin

90
Q

what are some ADRs of nitrofurantoin

A

darken urine
GI upset (take with food) `

91
Q

this medication has an MOA of inhibiting cell wall synthesis. it also decreases the adherence of bacteria to the epithelial cells of the urinary tract

A

fosfomycin

92
Q

what are some ADRs of fosfomycin

A
  • headache
  • diarrhea
  • GI upset
  • hypokalemia
93
Q

this medication works by passive diffusion into the cytoplasm of anaerobic bacteria. results inhibition of DNA synthesis and degradation and ultimately bacterial death; it is used for anaerobic and parasitic infections

A

metronidazole

94
Q
A