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HDID 2 > 30. Intro to antimicrobials > Flashcards

30. Intro to antimicrobials Flashcards

1
Q

do you want drugs with a high or a low therapeutic index?

A

high (ie toxic concentration is much higher than the concentration necessary to kill the bug)

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2
Q

properties of good antimicrobials?

A

high therapeutic index

desirable spectrum of activity

low potential for resistance

favorable Rx properties

low cost

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3
Q

why are all antimicrobials considered toxic?

A

decimate microbiota, select for resistant microorganisms, and can have adverse effects on other patients (global rise of antimicrobial resistance) EVERY TIME YOU USE ONE

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4
Q

what class of drugs target RNA pol?

A

rifamycins

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5
Q

what class of drugs target cell wall?

A

penicillins, cephalosporins, glycopeptides

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6
Q

what class of drugs are 30S ribosome inhibitors?

A

aminoglycosides, tetracyclines

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7
Q

what class of drugs are 50S ribosome inhibitors?

A

macrolides, oxazolidonones

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8
Q

what class of drugs inhibit intermediary metabolism?

A

trimethoprim, sulfonamides

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9
Q

what class of drugs target cell membrane?

A

lipopeptides

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10
Q

what class of drugs target topoisomerase?

A

quinolones

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11
Q

when to use broad vs narrow spectrum abx?

A

broad if don’t know organism or for polymicrobial infections

narrow if know causative agent via cultures

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12
Q

bacteriostatic vs bacteriocidal?

A

bacteriostatic:

  • stops growth
  • MBC&raquo_space;> MIC

bactericidal:

  • results in 99.9% reduction in number of organisms
  • MBC achievable

often unnecess to kill bug completely, because once you slow it down, the adaptive and innate immune systs will take care of it. Endocarditis is an exception because it is in a privilaged site, or ppl taking bactericidal antibiodics when have no neutrophils (chemo) or for treating meningitis

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13
Q

intrinsic vs acquired resistance?

A

intrinsic: drug was never effective vs bug
- can’t get in
- target different or absent

acquired: most isolates formerly susceptible
- may no longer be true
- genetic change
- selected by time
- theoretically reversible

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14
Q

steps in folate synthesis?

A

PABA (bacteria only)

dihydropteroic acid (thanks to dihydropteroate synthetase, inhib by sulfonamides)

dihydrofolic acid

tetrahydrofolic acid (thanks to dihydrofolate reductase, inhibi by trimethoprim)

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15
Q

sulfonamides are usually used in combo with what? why?

A

sulfamethoxazole (TMP - SMX, co-trimoxazole)

enhances activity (synergy), bactericidal vs many microbes, decreases emergence of resistance

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16
Q

TMP-SMX use?

A

broad activity

  • vs gram negatives
  • increasingly used vs S. aureus
  • active vs some protozoa and fungi
  • (pseudomonas, most enterococci resistant)

excellent bioavailability (gets into prostate and CSF no problemo)

excellent tissue penetration

  • excreted unchanged in urine (so used for UTIs)
  • penetrates prostate, CSF

used for infections of urinary, respiratory (esp sinusitis and otitis media) and GI tracts

increasing use for skin and soft tissue infections due to increasing resistance of S.aureus to other agents

inexpensive

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17
Q

TMP-SMX resistance?

A

TMP:
- acquisition of plasmid encoding alternate dhfr gene
- often transposon (Tn7) or part of integrons
(resistance in E.coli is now common, resistance in S. aureus is uncommon)

sulfonamides

  • can be due to chromosomal mutation
  • acquistion of a plasmid encoding alternative alleles of gene encoding dihydropteroate synthetase
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18
Q

TMP-SMX adverse effects

A

common

  • rash
  • nausea, vomiting, diarrhea

less common

  • hyperkalemia (high doses or renal insufficiency)
  • hepatitis, pancreatitis

severe (rare)

  • stevens-johnson syndrome and TEN (toxic epidermal necrolysis)
  • aplastic anemia, thrombocytopenia, anemia
  • hyemolytic anemia (G6PD deficiency)

pregnancy

  • kernicterus (late in pregnancy due to SMX)
  • early in pregnancy TMP is teratogenic

drug interactions
- displaces warfarin, phentoin, others from albumin

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19
Q

TMP-SMX route of admin

A

PO or IV BID or qD

20
Q

DNA gyrase?

A

topoisomerase II (gyrA and gyrB) creates supercoils

forms transient covalent bond to DNA via phospho-tyrosine

21
Q

topoisomerase IV?

A

(parC and parE) - de concatenates intertwined chromosomes

form transient covalent bond to DNA via phospho-tyrosine

22
Q

quinolones mechanism?

A

stabilize the enzyme(topoisomerase)-DNA complex w/dsDNA breaks

interferes w/ DNA rep and RNA txn

eventual chromosome fragmentation results in lethality

23
Q

all quinolones have broad activity vs what?

A

gram- bacteria (gyrase/Topo II inhibition impt) and atypicals (mycoplasma, chlamydia, legionella) and mycobacteria

24
Q

ciprofloxacin has relatively poor activity vs what? (making it apoor drug for respiratory infections)

A

streptococci

25
Q

gram+ activity of quinolones requires what?

A

Tpop IV inhibiiton

26
Q

bioavailability of quinolones?

A

good orally, but poor absorption in presence of divalent cations (antacids, Fe, Zn)

most excreted in urine except for moxifloxacin

long half-lives for BID or qD dosage

27
Q

ciprofloxacin targets what?

A

DNA gyrase, concetrated in urine so used for UTIs

28
Q

moxifloxacin targets what?

A

gram+ and anaerobic activity - pneumonia, mycobacterial infectoins, polymicrobial (anaerobic) infections

29
Q

fluoroquinolone resistance?

A

across class, can develop during therapy

mutations in taget enzyme

  • gyrA or parC near active site tyrosine
  • differ by org (single mutation in S. aureus, double in E.coli, global E.coli clone now!)

efflux pumps
- derepression of MDR transporters (evolved to have high level expression)

30
Q

Fluoroquinolone adverse effects?

A

safe

nausea, vomiting, abd pain, headache, dizziness

can prolong QT interval in combo w/other drugs

tendon rupture

potential for arthropathy in children?

31
Q

mechanism of Nitrofurantoin action?

A

DNA inhibitor

32
Q

nitrofurantoin spectrum of activity?

A

active vs gram+ and gram- uropathogens including Staph saprophyticus, strep agalactiae, enterococcus faecalis, E. faecium, E.coli, Klebsiella pneumoniae

NOT vs proteus spp,, pseudomonas spp., or serratia marcescens

33
Q

pharma properties of nitrofurantoin?

A

admin PO, does not reach adequate serum levels, but concentrated in urine

34
Q

use for nitrofurantoin?

A

UTI

35
Q

adverse effects of nitrofurantoin?

A

nausea is common

pulmonary fibrosis rare (occurs w/chronic use)

36
Q

rifamycins mechanism?

A

bind to B subunit of RNA polymerase and block txn

bacteriostatic

37
Q

resistance of rifamycins?

A

evolves rapidly due to mutations in binding pocket super frequently

frequently preexist in the population, which limits effectivenes

38
Q

rifampin specific side effects?

A

turns urine/secretions orange

potent inducer of P450 3A4, so increases metabolism of many drugs

39
Q

rifabutin specific side effects?

A

levels can rise in presence of inhibitors of p450 3A4 (like macrolide antibiotics)

40
Q

rifaximin use?

A

GI only (not absorbed)

41
Q

rifamycins use?

A

for prophylaxis:
- eradicate carriage of Neisseria meningitidis, S. aureus

in combo w/other antimicrobials

  • mycobacterial infections
  • for synergy in serious bacterial infections

for GI infections (rifaximin only)

42
Q

rifamycins adverse effects?

A

GI (pain, nausea, vomiting, diarrhea)

hematological (mild thrombocytopenia, leukopenia, anemia)

hepatitis (w/other drugs or pre-existing liver disease)

43
Q

fidaxomicin mechanism

A

blocks RNA pol by preventing formation of open DNA complex

44
Q

fidaxomicin side effects?

A

none reported

45
Q

fidaxomicin use?

A

poor activity vs Gram- enteric flora including gram- anaerobes

approved only for C.diff infections (w/ fewer relapses than vancomycin)

but super expensive

HDID 2 (32 decks)

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