Antimicrobial Chemotherapies Flashcards

(71 cards)

1
Q

what are chemotherapeutic agents?

A

chemical agents used to treat disease that destroy pathogenic microbes or inhibit their growth within the host

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

what are most chemotherapeutic agents classified as?

A

antibiotics

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

what are antibiotics?

A

microbial products or their derivative that kill susceptible microbes or inhibit their growth

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

how was penicillin discovered?

A

accidentally by Alexander Fleming
observed penicillin activity on a contaminated plate but did not think it could be developed further

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

what is selective toxicity?

A

ability of a drug to kill or inhibit a pathogen while damaging the host as little as possible

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

what is a therapeutic dose?

A

drug level required for clinical treatment

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

what is a toxic dose?

A

drug level at which drug becomes too toxic for the patient

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

what is the therapeutic index?

A

ratio of toxic dose to therapeutic dose

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

what are side effects?

A

undesirable effects of drugs on host cells

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

what are narrow spectrum drugs?

A

attack only a few different pathogens

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

what are broad spectrum drugs?

A

attack many different kinds of drugs

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

what do cidal agents do?

A

kills the target pathogen

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

what do static agents do?

A

reversibly inhibits growth of microbes

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

how does the effect of an agent vary?

A

with concentration, microbe, and host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how is effectiveness expressed? (2 ways)

A

minimal inhibitory concentration and minimal lethal concentration

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

what is minimal inhibitory concentration?

A

lowest concentration of drug that prevents growth of the pathogen

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

what is the minimal lethal concentration?

A

lowest concentration of drug that kills the pathogen

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

what are the main modes of action of antimicrobial drugs?

A

inhibitors of cell wall synthesis
protein synthesis inhibitors
metabolic antagonists
nucleic acid synthesis inhibition

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

how does chromosome replication and partitioning occur?

A

most bacteria have a single circular chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the single origin of replication?

A

site at which replication begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the terminus?

A

site at which replication is terminated, located opposite of the origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the replisome?

A

group of proteins needed for DNA synthesis?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is septation?

A

formation of cross wall between two daughter cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the steps of sepatation (cytokinesis)?

A

selection of site for septum formation
assembly of Z ring (composed of protein FtsZ)
assembly of cell wall-synthesizing machinery
constriction of cell and septum formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is the main protein of interest in septation?
FtsZ
26
what are the steps of cell wall synthesis?
fliptadase moves the bactoprenol across the membrane and attaches to and moves the NAG-NAM complexes glycosyltransferase joins all of the sugar layers together transpeptidase (penicillin binding protein) attaches the amino acid chains and brings the layers together
27
would cell wall synthesis inhibitors work better against gram positive or gram negative bacteria?
gram positive because there is not the protection of the outer membrane that is present in gram negative cells
28
what is the most crucial feature of penicillin?
B-lactam ring
29
why is the B-lactam ring so important?
essential for bioactivity
30
what makes penicillin resistant organisms resistant?
many penicillin resistant organisms produce B-lactamase which hydrolyzes a bond in the ring
31
what is the mode of action for penicillin?
blocks the enzyme that catalyzes transpeptidation (formation of cross-links in peptidoglycan) prevents the synthesis of complete cell walls leading to lysis of cell acts only on growing bacteria that are synthesizing new peptidoglycan
32
what kind of penicillin is narrow spectrum?
penicillin V and G are narrow spectrum
33
why do semisynthetic penicillins have a broader spectrum than naturally occurring ones?
bulkier side chains make them more difficult for B-lactamase enzymes to degrade
34
what can include in an antibiotic to increase efficiency?
B-lactamase inhibitors
35
what are the characteristics of cephalosporins?
structurally and functionally similar to penicillin broad spectrum antibiotics that can be used by most patients that are allergic to penicillin there are four categories based on their spectrum of activity
36
what are the characteristics of vancomycin?
glycopeptide antibiotic inhibits cell wall synthesis vancomycin- important for treatment of antibiotic-resistant staphylococcal and enterococcal infections previously considered "drug of last resort" so rise in resistance to vancomycin is of great concern
37
what do protein synthesis inhibitors do?
bind to the bacterial ribosome
38
what are the four steps that can be targeted by PSIs?
aminoacyl-tRNA binding peptide bond formation mRNA reading translocation
39
aminoglycoside characteristics
large group, all with a cyclohexane ring, amino sugars bind to the 30S ribosomal subunit, interfere with protein synthesis by directly inhibiting the process and by causing misreading of the messenger RNA
40
tetracycline characeristics
all have a four-ring structure to which a variety of side chains are attached broad spectrum, bacteriostatic target the 30S subunit of the ribosome that inhibits protein synthesis
41
macrolide characteristics
contain 12- to 22- carbon lactone rings linked to one or more sugars ex: erythromycin broad spectrum bacteriostatic binds to 50S ribosomal subunit to inhibit bacterial protein elongation used for patients allergic to penicillin
42
metabolic antagonists characteristics
act as antimetabolites and are structural analogs
43
what are antimetabolites?
antagonize or block functioning of metabolic pathways by competitively inhibiting the use of metabolites by key enzymes
44
what are structural analogs?
molecules that are structurally similar to, and compete with, naturally occurring metabolic intermediates to block normal cellular metabolism
45
sulfonamide drug characteristics
structurally related to sulfanilamide, a para aminobenzoic analog, which are used for the synthesis of folic aid and is made by many pathogens makes them selectively toxic due to the competitive inhibition of folic acid synthesis
46
trimethoprim characterisitics
synthetic antibiotic that also interferes with folic acid production broad spectrum can be combined with sulfa drugs to increase efficacy of treatment -combo blocks two steps of the pathway
47
what are the two most commonly used antibacterials drugs that inhibit nucleic acid synthesis?
fluroquinolones rifamycins
48
why ae nucleic acid synthesis targeting drugs not as selectively toxic?
because bacteria and eukaryotes fo not differ greatly in the way they synthesize nucleic acids
49
fluoroquinolone characteristics
synthetic drugs that contain a 4-quinolone ring act by inhibiting bacterial DNA gyros and topoisomerase II broad spectrum, bactericidal, treat a wide variety infections
50
what does bacitracin do?
inhibits dephosphorylation
51
what does furazolidone do?
block DNA transcription
52
what does optochin do?
interferes with ATPase and ATP production
53
why has antiviral drug development been slow?
because it is difficult to specifically target viral replication bc many target cells are similar to our celss
54
tamiflu
anti-influenza agent neuraminidase inhibitor shortens course of illness
55
what are nucleoside reverse transcriptase inhibitors?
anti-HIV drugs that target and interfere with critical steps in viral replicative processes
56
what are non nucleoside reverse transcriptase inhibitors?
prevent HIV DNA synthesis by selectively binding to and inhibiting the viral reverse transcriptase enzyme
57
protease inhibitors
block the activity of the HIV protease needed for the production of all viral proteins
58
integrase inhibitors
present the incorporation of the HIV genome into the host's chromosomes
59
fusion inhibitors
prevent HIV entry into cells
60
what is the most successful way to avoid resistance with HIV drugs?
drug cocktails
61
antifungals
fewer effective agents because of similarity if eukaryotic fungal cells and human cells many have low therapeutic indexes and are toxic
62
superficial mycoses
Candida topical and oral disrupt membrane permeability and inhibit sterol synthesis disrupts the mitotic spindle; may inhibit protein and DNA synthesis
63
systemic mycoses
difficult to control and can be fatal
64
what are the three common drugs to treat systemic mycoses?
amphotericin B-binds sterols in membrane 5-flucytosine-disrupts RNA function fluconazole- low side effects, used prophylactically
65
examples of antiprotozoan drugs
quinine (chloroquine and mefloquine)-malaria metronidazole- entamoeba
66
what are the three types of drug resistance?
intrinsic acquired drug-tolerant
67
intrinsic resistance
mycoplasma resistance to B-lactam antibiotics and other cell wall inhibitors because they lack a cell wall
68
acquired resistance
occurs when there is a change in the genome of a bacterium that converts it from one that is sensitive to an antibiotic to one that is resistant i.e, plasmids
69
drug tolerant resistance
bacteria lacks the mechanisms for antibiotic resistance and ignore the presence of antibiotics ex: bacteria embedded in biofilms
70
what are the 4 mechanisms of drug resistance?
modify the target of the antibiotic drug inactivation using the enzyme from a plasmid minimize the concentration of antibiotic in the cell by pumping them out bypass the biochemical reaction inhibited by the agent or increase the production of the target metabolite
71
how can we overcome drug resistance?
give the drug in appropriate concentrations to destroy susceptible microbes and most spontaneous mutants give two or more drugs at a time use drugs only when necessary continue development of new drugs possibly use bacteriophages to treat disease