Final Flashcards

1
Q

The use of drugs to treat a disease

A

chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

interfere with the growth of microbes within a host

A

Antimicrobial drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

of biological origin. produced by a microb, inhibits other microbes

A

Antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

synthetic chemicals

A

chemotherapeutic agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Today distinction -> many newer antibiotics are biological products that are

A

chemically modified or

chemically synthesized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ddrugs kills pathogens without damaging the host

A

selective toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ratio between toxic dose and therapeutic dose or ration of LD50 to ED50

A

therapeutic index

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

high therapeutic index

A

less toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bacteriostatic vs. bactericidal - range of activity of an antimicrobial against bacteria

A

antimicrobial action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

broad-spectrum vs. narrow spectrum

A

activity spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

BBB, unstable in acid; half-life duration

A

tissue distribution, metabolism, and excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

combinations of two antibiotics that have enhanced bactericidal activity when tested together compared with the activity of each antibiotic; to prevent the emergence of of resistant organisms during therapy

A

antibiotic synergism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

combination of antiobiotics in which the activity of one antibiotic interferes with the activity of the other

A

antibiotic antagonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ideal drug

A
There is no ideal drug
but
selective toxicity
lack of side effect
bactericidal vs. bacteriostatic
favorable pharmacokinetics
spectrum of activity
little resistance development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

selective toxicity

A

against target pathogen but not against host

LD high vs. MIC and/or MBC(low)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lack of side effects

A

therapeutic index:effective to toxic doees ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

favorable pharmacokinetics

A

reach target site in body with effective concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

spectrum of activity

A

broad vs. narrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

susceptibility test

A
  1. broth dilution
  2. agar dilution
  3. agar diffusion –> kirby-bauder disk diffusion test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

zones of inhibition depend upon

A
pH of environment
media components (agar depth, nutrients)
stability of drug
size of inoculum
length of incubation
metabolic activity of organism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  1. inhibition of cell wall synthesis
A

penicillins, cephalosporins, bacitracin, vanomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  1. inhibition of protein synthesis
A

chloramphenicol, erythromycin, tetracyclines, streptomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  1. inhibition of nucleic acid replication and transcription
A

quionolones, rifampin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
  1. injury to plasma membrane
A

polymyxin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
  1. inhibition of synthesis of essential metabolites
A

sulfanilamide, trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

antimicrobials of class 1 (wall)

A

beta lactam drugs

non-beta latam drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

beta lactam drugs

A

penicillins and cephalosporins

28
Q

penicillins are more effective against?

A

gram posistive bacteria because it has penicillin binding proteins on their walls

29
Q

cephalosporins are most effective against?

A

Gram negative

currently working with 5th generation cephalosporins

30
Q

bacitracin

A

non beta lactams
inhibit cell wall
mycobacterial infections

31
Q

cycloserins, ethiionamide and isoniazid

A

interferes with transport of peptidoglycan precursors across cytoplasmic meembrane
non-precription first aid

32
Q

vancomycin

A
cell wall 
inhibit formation of glycan chains
gram - innately resistnat
so effective in gram +
intravenously 
alternation of side chain of NAM
USED TO KILL MRSA
resistance: VRE and VRSA
33
Q

Inhibition of protein synthesis 4 drugs?

A

aminoglycosides
tetracyclins
macrolids
chloramphenicol

34
Q

aminoglycosides

A

effective in gram negative
Irreversible binds to 30S
synergistic combination with beta lactam drugs

35
Q

aminoglycosides examples?

A

gentamicin, streptomycin, tobramycin, amikacin, kanamycin, spectinomycin, neomycin

36
Q

side ieffects of aminoglycosides?

A

ototoxicity,nephrotoxicity

37
Q

tetracyclins

A

reversibly bind to 30S
effective Gram - and +
dexycycline have longer half life
cause discoloration of teeth for young child
resistnace due to decreased accumulation by bacterial cell

38
Q

Macrolides

A

reversibly binds to 50S
Gram +
for atypical pneumonia
choice for patiens allergic to penicilin

39
Q

macrolides examples?

A

erythromycin, clarithromycin and azithromycin

40
Q

chloramphenicol

A

binds to 50S
effective against a wide variety of organisms
last resort for life threatening infecctinos
lethal side effect is aplastic anemia

41
Q

Inhibition of DNA RNA synthesis, 2types?

A

Fluoroquinolones and Rifamycin

42
Q

Fluoroquinolones

A

inhibit action of topoisomerase DNA gyrase
effective Gram + and -
ex) ciprofloxacin and ofloxacin

43
Q

rifamycins

A

block prokaryotic RNA polymerase
most widely used
effective Gram + and - and also Mycobacterium

tuberculosis and hansen’s disease, meningitis
resistnace develops rapidly

44
Q
  1. injury to plasma membrane 2?
A

Polymxin B and colistin
common first aid skin ointment
Gram -

45
Q
  1. inhibition of synthesis of essential metabolite, 2 types?
A

Sulfonamides and Trimethoprim

46
Q

Sulfonamides

A

Gram - and +
similar to paraaminobenzoic acid
human cells lack specific enzyme in folic acid pathway-> selective toxicity

47
Q

trimethoprim

A

inhibits folic acid production

used synergically with sulfonamide

48
Q

Mechanisms of resistance non genetic

Drug inactivating enzymes

A

penicilinase
chloramphenidol acetyl transferase
aminoglycosides and transferases

49
Q

Mechanisms of resistance non genetic

alteration of target molecule

A

Rifampicin
naladixic acid
streptomycin
erythromycin

50
Q

Rifampicin

A

altered RNA polymerase(mutants)

51
Q

Naladixic acid

A

altered DNA gyrase

52
Q

Streptomycin

A

altered ribosomal protein

53
Q

erythromycin

A

methylation of 23S rRNA

54
Q

Mechanisms of resistance non genetic

decreased uptake of the drug

A

alteration in porin protein decrese permeability of cells

55
Q

Mechanisms of resistance non genetic

increased elimination of the drug

A

some organisms produce efflux pumps

capacity to eliminate drug
resist higher con. of drug
tetracycline resistance

56
Q

Mechanisms of resistance-non general

metabolic inactivity

A

mycobacterium dormancy

57
Q

loss of target

A

penicillin non-growing cells; L-forms

58
Q

intrinsic resistance

A

naturally insensitive

59
Q

antimicrobial resistance genetic mechanism 4of them?

1spontaneous mutation of old gene

A

vertical evolution

60
Q

antimicrobial resistance genetic mechanism

2acquisition of new genes

A

horizontal evolution

61
Q

antimicrobial resistance genetic mechanism 4of them?

A

1spontaneous mutation of old gene
2acquisition of new genes
3. chromosomal resistance
4. extrachromosomal resistance

62
Q

antimicrobial resistance genetic mechanism

4. extrachromosomal resistance

A

integrons, transposons, plasmid

63
Q

antimicrobial resistance genetic mechanism

  1. extrachromosomal resistance
    - plasmids, what kinds?
A

multiple genes/plasmid
restricted or broad host range
transfer between cells (conjugation due to tra genes/ non-conjugal - transcution and comobilization of conjugation plasmids)

64
Q

Misuse of antibiotics includes?

A

using oudated or weakened antibiotics
using a ntibiotics for the common cold and other inappropriate condition
using antibiotics in animal feed
failing to complete the prescribed regiment
using someone else’s leftover prescription

65
Q

Household halogenated antibicrobial agents?

A

inhibit bacterial growth
purpose is to prevent transmission of disease-causing microbes to non-infected person in clinical settings
improper use can select for resistant strains

66
Q

triclosan studies?

A

effect diluted by water
one gene mutation for resistance
contact time exceeds normal hand wash time (5 sec)
allergies

67
Q

Next threat to humanity

A

multidrug-resistant mycobacterium tuberculosis