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IBI Test 1 > B3.010 Introduction to Antimicrobial Chemotherapy > Flashcards

B3.010 Introduction to Antimicrobial Chemotherapy Flashcards

1
Q

what are the 4 qualities a drug must have to be effective?

A
  1. get where its needed
  2. in an active form
  3. in a sufficient quantity
  4. for a sufficient time
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2
Q

absorption

A

defines routes of administration

special considerations given to speed, reliability, and compliance

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3
Q

what are some important things to consider when examining drug distribution?

A

reliability
important of blood and tissue levels in therapeutic and toxic effects
entry into mammalian cells

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4
Q

what are some sites of exclusion of drug distribution?

A 
blood/brain barrier
ocular fluid
synovial fluid
pleural fluid
cysts (physical barrier)
necrotic tissue (physical barrier)
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5
Q

why is metabolism important?

A

host metabolism is not important for many anti-microbials, but required for some antivirals
metabolism by pathogen may be a key determinant of activity and specificity

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6
Q

what % of chemotherapeutic agents are toxic?

A

all of them

100%

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7
Q

what is the goal of chemo?

A

selective toxicity targeting a pathogen rather than the host

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8
Q

how is selective toxicity achieved?

A
  1. unique target present in pathogen and absent in host
  2. target structurally different in pathogen than in host
  3. target more essential in pathogen than in host
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9
Q

what are some of the targets for selective toxicity?

A 
cell wall synthesis (good bc mammalian cells don't have cell walls)
membrane integrity
protein synthesis 
nucleic acid synthesis
nucleic acid integrity
cytoskeleton integrity
lipid synthesis
energy production
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10
Q

when targets are not unique to pathogen, what may enhance selective toxicity?

A

fundamental differences between species and cell types

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11
Q

what are the major classes of anti-bacterial drugs

A 
A. cell wall synthesis inhibitors
B. membrane affectors
C. Inhibitors of protein synthesis
D. Folate inhibitors
E. DNA gyrase inhibitors
F. Urinary tract antiseptics
G. Anti- mycobacterial drugs
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12
Q

what are the sub classes of cell wall synthesis inhibitors?

A
  1. penicillins
  2. cephalosporins
  3. other B-lactams
  4. other inhibitors
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13
Q

what are the sub classes of inhibitors of protein synthesis?

A
  1. tetracyclides
  2. macrolides
  3. aminoglycosides
  4. other inhibitors
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14
Q

what are the sub classes of folate inhibitors?

A
  1. sulfonamides

2. reductase inhibitors

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15
Q

what are the sub classes of DNA gyrase inhibitors?

A
  1. fluoroquinolones
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16
Q

what are the 5 key features of pharmacodynamics for chemotherapeutic drugs?

A
  1. mechanism of action
  2. spectrum of activity
  3. static vs cidal
  4. development/incidence of resistance
  5. role of host defenses
17
Q

what do cyto- or bacterio-static drugs do?

A

inhibit growth and proliferation

18
Q

what do cyto- or bacterio-cidal drugs do?

A

kill pathogens

19
Q

are static or cidal drugs prefereed in immunocompromised patients?

A

bacteriocidal

20
Q

what happens when you combine bacteriostatic drugs?

A

can have a bacteriocidal effect

synergy

21
Q

how does the role of host defenses combine with chemo?

A

chemotherapy seldom produces a cure directly
host immune function usually provides the final cure
in immunocompromised patients, bactericidal agents usually are more effective

22
Q

what is time dependent killing?

A

used by pens, cephs, vancomycin
time above MBC relates to efficacy
MBC = minimum bactericidal concentration

23
Q

what is concentration dependent killing?

A

used by aminoglycosides, fluoroquinolones
peak serum concentration relates to the extent of killing
higher peak values result in increased efficacy and decreased development of resistance

24
Q

what are some things that would have been impossible without antimicrobial drugs?

A 
joint replacement
organ transplant
cancer chemotherapy
high survival rates for premature infants
ICUS
25
Q

describe how resistance develops

A

only pathogens sensitive to a given drug or combination of drugs will be affected
resistant pathogens will then enjoy a selective advantage for growth and proliferation
selection for resistance is rapid and reversibility is slow/non-existent

26
Q

what facilitated the emergence of resistance?

A

misuse, overuse
overuse of broad spectrum drugs
global society
decline in antimicrobial drug development

27
Q

antibiotic stewardship

A

treat infections only when benefit outweighs individual and global risks
bronchitis, sinusitis, otitis media overall show little benefit from antibacterial therapy

28
Q

what are general mechanisms for resistance?

A
  1. pathogen does not absorb drug
  2. pathogen pumps drug out
  3. pathogen metabolism inactivates drug
  4. modified target in pathogen not affected by drug
  5. increased production of target molecules
  6. development of altered metabolic pathways to bypass target
29
Q

what is non-genetic (temporary) resistance?

A

pathogen may be metabolically inactive, or dormant

30
Q

what are 2 forms of genetic (permanent) resistance?

A

chromosomal
-based on mutation in gene coding for target
-lose effect of drug but maintain normal function
-pass on to progeny
extrachromosomal
-based on addition of plasmid to pathogen
-plasmids may carry multiple genes providing multiple drug resistance
-plasmids may be passed on to other cells without proliferation

31
Q

how can you minimize the emergence of resistance?

A

only use chemotherapeutic agents when they are clearly indicated
use narrow spectrum drug known to be effective against the pathogen which is present
use an effective dose of the chemotherapeutic agent
consider the patient’s phenotype/genotype in establishing dosing regimen
ensure that the duration of chemo is adequate
use older drugs when possible
use multiple drugs in combination chemo when the pathogen is noted to develop resistance to an individual drug rapidly

32
Q

what is a superinfection?

A

appearance of a new, often more severe, infection as a result of primary chemotherapy
alter normal flora and see overgrowth of other microorganisms
often GI

33
Q

how can you distinguish a superinfection from direct irritation by the drug?

A

time course

superinfections take longer to develop and then occur all of a sudden

34
Q

what are the 3 major glasses of GI superinfections?

A
  1. candidiasis
    - fungal
    - most common
    - continue antibacterial, add antifungal
  2. staphylococcal enterocolitis
    - life threatening
    - discontinue anti-bac
    - administer anti staph penicillin or vancomycin
  3. pseudomembranous colitis
    - life threatening
    - c.diff
    - discontinue antibacterial
    - administer metronidazole or vancomycin
35
Q

what are 3 primary adverse effects of chemotherapy?

A
  1. toxicity to host
    - dose related
    - often related to mechanism of action
  2. hypersensitivity
    - immune mediated toxicity
    - not related to dose
  3. idiosyncratic responses
    - may be genetically determined
    - may reflect altered pharmacokinetics
36
Q

indications for combination chemotherapy

A
  1. for enhanced effect (synergism)
  2. to allow for lower doses or individual drugs to minimize toxicity for the patient
  3. to delay development of resistance
  4. for the treatment of mixed infections
  5. to initiate therapy in life threatening situations when the pathogen is not known
37
Q

indications for chemoprophylaxis

A
  1. to protect healthy individuals following exposure to specific pathogens
  2. to minimize active, symptomatic episodes of chronic infections
  3. to prevent post surgical infections
  4. to prevent bacterial endocarditis
38
Q

drug selection in chemotherapy in 4 steps

A
  1. can the drug affect the pathogen?
  2. are the pharmacokinetics of the drug appropriate?
  3. is the drug appropriate for the patient?
  4. is the drug ideal?

IBI Test 1 (15 decks)

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