Antibiotics 1 and 2 Flashcards

1
Q

how was penicillin discovered

A

1928- dr felming notices that the mold penicillium prevented normal growth of saphylococci

1941- alternative strain of penicillium chyrosogeium which yielded 200x amount of penicilin

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2
Q

first pt treated w/ peniccilin

A

1942- anne miller treated w/ penicillin

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3
Q

ideal antibiotics

A

target one or more bacterial species w/ no toxicity or allergy

effective concentration at sites of infection, absorption, distribution, metabolism, excretion

persist long enough to destroy target

overcome bacterial resistance

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4
Q

pharmacokinetics

A

what the body does to the drug

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5
Q

pharmacodynamics

A

toxicity and therapeutic index (Lethal Dose/Effective Dose)

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6
Q

two major mechanisms of antibiotic action

A

bacertiostatic- prevents growth but does not kill bacteria. removal of drug results in resumed growth

bacteriacidal- kills bacteria. drug is removed when bacteria is dead

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7
Q

large therapeutic index

A

over 10

indicates a large window where the drug can be safely used

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8
Q

methods for determining the efficacy of antibiotics in vitro

A

kirby bauer disc diffusion essay- testing multuple antibiotics ability to kill a pathogen. culture a plate of bacteria and add antibiotics to plate. incubate overnight. measure the diamater of the zone of inhibition. only tests for inhibitory concentrations

MIC- minimal inhibitory concentration (minimal amount of antibiotic required to inhibit growth). done by diluting the amount of antibiotic in a bacterial culture to find minimum necessary amount. alternatively, can use e-test as a quick version w/ antibiotic gradient

MBC- minimal bactericidal concentration (minimal amount of antibiotic to kill the bacteria). done by plating MIC results to see if they grow.

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9
Q

describe the MBC/MIC ratio in bacteriostatic and bactericidal drug

A

static- high

cidal- low

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10
Q

properties of antibiotics that must be considered before use

A

bacteriostatic vs bacteriocidial

therapautic range (low can e toxic)

resistance

drug penetration at infected sites

factors that affect drug distribution (absorption, distributoin, metabolism, and excretion)

toxicity

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11
Q

characterisitics of the patient that are important when considering antibiotics

A

route of administration

duration of treatment

age, sex, general health, concurrent medication and disease, allergies, immunological status

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12
Q

what are the mechanisms of antibiotics?

A
  1. inhibition of cell membrane synthesis
  2. inhibition of cell wall synthesis
    3 inhibition of bacterial protein synthesis
    4 inhibition of nuclei acid synthesis
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13
Q

drugs that affect cell membrane synthesis

A

lincomycins
daptomycin
polymixin

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14
Q

drugs that affect bacterial protein synthesis

A

aminoglycosides- 30S ribosome
tetracyclines- 30S ribosome

chloramphenicol- 50S ribosome
macrolides- 50S ribosome
clindamycin- 50S ribosome

mupirocin- tRNA

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15
Q

antimetabolites

A

analogs that interfere w/ synthesis or function involved in cell metabolism

sulfonamide- group of compounds w/ structure to PABA that interferes w/ folic acid metabolism (prevents production of dihydropteric acid, an intermediate of THF) (static)

trimethoprim- prevents last step in folic acid metabolism, used in conjuction w/ sulfonamide (inhibits DHF reductase, which binds 1000x more strongly to bacterial DHF) (cidial)

isoniazid- bactericidal drug that destroys integral component of mycobacterial cell wall (cidial)

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16
Q

are antimetabolites static or cidal?

A

static- interfere w/ folic acid metabolism which inhibits DNA synthesis

17
Q

bactrim

A

antimetabolite which is the combination of sulfamethoxazome and trimethoprim

used for UTIs

18
Q

B- lactam antibiotics

A

anti-cell wall antibiotics
penicillin- uses its b-lactam ring to bind the penicillin binding protein necessary for the transpepitdation rxn that creates the cross linking in cell walls

synthetic penicillins- methicillin, oxacillin, cephalosporins

more effective in combination w/ b-lactamase inhibitors (augmentin)

19
Q

when is penicillin effective?

A

cells must be growing and dividing for penicillin to be effective

20
Q

penicillin g vs v vs vk vs ampicillin

A

K- sensitive to acid hydrolysis- only for IV or IM

sensitive to B-lactamases

active against Gram+, not gram

V and VK- resist acid hydrolysis- taken orally

ampicillin/amoxicillin- amino penicillin- resists acid hydrolysis, has a broader spectrum (w/ some Gram - efficacy)

21
Q

synthetic penicillins

A

sensitive to penicllinase, broader spectrum

  • ampicilin- acid stable
  • amoxicillin (higher serum levels) acid stable

sensitive to penicillinase, extended spectrum

  • tricarcillin
  • piperacillin - most effective against G- entero bacilli

resistant to penicllinase, less active against G+, no G-

  • methicllin (acid labile)
  • oxacillin- acid resistant
22
Q

carboxypenicillins

A

tricarcillin, pipeacillin, carbenicillin

extended spectrum into Gm -, but decreased Gm+ efficacy

23
Q

cephalosporins

A

similar to structure w/ B-lactam ring, bacteriocidal, but w/ a different R group (has dihydrothiazine)

broader spectrum
greater acid stability
resistant to B-lacamases
cross rxn w/ penicillin allergy

24
Q

monobactams

A

aztereonam

monocyclic b-lactam

b-lactamase resitant
active against aerobic Gm- bacteria
generally inactive against Gm + or anerobes

25
Q

carbapenems

A

imipenem or meropenem

resistant to b-lactamases

broadest spectrum, most effective against gram - bacteria

26
Q

b-lactamse inhibitors

A

used in combination w/ b-lactam antibiotics

clavulonic acid- in combination with amoxicillin (augmentin- oral)

sulbactam - in combination w/ ampicillin (unasyn- parenteral)

tazobactam- in combination w/ piperacillin (zosyn IV)

27
Q

glycopeptide cell wall synthesis inhibitors

A

vancomysin

talvancin

teicoplanin

28
Q

vancomysin

A

binds to D-ala-D-ala, restricted to gram +

nephrotoxicity

inhibits peptidoglycan precursor transfer

29
Q

vancomysin is the drug of choice for which infections?

A

multiple resistant enterococcus

methicllin resistant staph aureus (MRSA)

30
Q

cycloserine

A

inhibits cell wall synthesis

d-ala analogue, inhibits d-ala-d-ala cross link

TB secondary dr8gug

31
Q

bacitracin

A

inhibits cell wall synthesis

inhibits lipid carriers step. can only be used topically

gram + only

32
Q

drugs that inhibit cell wall synthesis

A
penicllins
vancomycin
telavancin
cephalosporin
monobactam
carbapenem
33
Q

drugs that inihibit nucleic acid synthesis

A
sulphonamides
trimethoprim- folic acid metabolism
metronidazole
quinolones- inhibit DNA gyrase
rifampacin- inhibit RNA polymerase
34
Q

cephalospore generatoins

A

1st- effective against Gm+ and some -. not PA
cephazolin

2nd- effective against Gm + and -, not PA
cefuroxime

3rd- increased B-lactamse resistance, Gm + and -, effective against Pa

ceftriaxone, ceftazidime