Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

D&D Infectious Disease Midterm > Pharm - Antimicrobial Intro Part 2 > Flashcards

Pharm - Antimicrobial Intro Part 2 Flashcards

1
Q

explain what broad spectrum antibiotics are

A

they’re used to treat MANY different types of infections bc they are active against a wide range of bacterial species

they target processes/structures that are common to MANY different bacteria - that’s how they can treat wide variety of infections

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

name a major disadvantage of broad spectrum antibiotics

A

commensal bacteria are much more susceptible to broad spectrum (over narrow)

not only can this cause side effects like diarrhea, but it can lead to superinfection - when all the good bacteria are killed and there’s still a few bad left -they can overgrow and infect again
(FINISH FULL COURSE!)

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

TRUE OR FALSE

narrow spectrum antibiotics may be discontinued once the infectious agent is identified

A

FALSE - this is true for broad

once you find out the agents you can switch to NARROW

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

narrow spectrum agents are effective against….

A

a single or just a few types of bacteria

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

narrow spectrum antibiotics are used when…..

A

the causative agent is KNOWN

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

how are narrow spectrum antibiotics able to target only a single or a few types of bacteria

A

because they target a SPECIFIC MOLECULE involved in bacterial metabolism (species specific)

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

which are more susceptible to developing resistance and why - broad spectrum or narrow spectrum

A

narrow spectrum is less likely to develop resistance because they’re not used as often as broad spectrum

the more you use, the more chance of resistance

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

which has higher incidences of superinfeciton - broad or narrow spectrum

A

broad spectrum because they kill more commensal bacteria and the pathogenic bacteria can overgrow

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

why are some antibiotics “reserved”

A

to prevent resistance to them

reserved for specific indications or certain resistance types when nothing else is working

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

what is another name for “empirical” antimicrobial therapies and explain

when is this done?

A

presumptive

given before the pathogen responsible for the illness OR the susceptibility to particular antimicrobial agent is known

done in cases of clinical experience - you know the signs and symptoms of certain infections, when early intervention is vital, when it’s difficult to identify the pathogen

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

what is “pre-emptive” antimicrobial therapy

A

given when high chance they’re infected, but not showing any symptoms

done in the army a lot of infection is spreading - given to all soldiers even if no symptoms (yet)

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

true or false

when giving empiric antimicrobial therapy, symptoms have already started showing

A

true

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

what is definitive therapy

A

when the pathogenic organism responsible for the illness has been identified, and the treatment is modified accordingly

dose could be lowered, completely switched to narrow spectrum, pharmacokinetic adjustments, etc

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

TRUE OR FALSE

in definitive therapy, the drug may be the same as the empiric therapy

A

true - dose may just be lowered or the empiric therapy may be changed completely

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

explain suppressive therapy

A

ie: HIV and herpes

the virus stays latent and the infection never goes away. therapy to suppress and prevent reactivation

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

name 3 pharmacokinetic considerations

A

patient factors

drug conc in body fluids

monitoring the serum concentrations of the antimicrobial agnets (esp if they can cause toxicities)

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

name 2 categories of combination antimicrobial therapy

A

synergism and antagonism

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

give 5 potential reasons for combination antimicrobial therapy

A

-broad-spectrum empiric therapy in seriously ill pts

-treat polymicrobial infections

-decrease emergence of resistant strains

-decrease dose-related toxicity bc can use lower doses of 1 or more components in regimen

-obtain enhanced inhibition/killing

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

as mentioned, combination antimicrobial therapy is sometimes used to decrease the emergence of resistant strains

give example

A

tuberculosis, HIV

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

name 3 drug-drug antimicrobial interactions that are SYNERGISTISC (just in general - not specific)

A

-blocking sequential steps in bacterial metabolic sequence

-inhibit inactivation by bacterial enzymes

-enhance the antimicrobial agent uptake by bacteria

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

explain how trimethoprim-sulfamethoxazole combination is an example of synergism

A

they block sequential steps in the same metabolic sequence/pathway of bacteria

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

what is sulbactam

A

a beta lactamase inhibitor

results in SYNERGISM when combined with beta lactam

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

true or false

sulbactam does NOT kill bacteria

A

TRUE

does not kill the bacteria - protects the drug from enzymes that the bacteria make to try to destory the antibiotic

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

3 examples of synergism (general)

A

-blocking sequential steps in a metabolic sequence

-inhibiting enzymatic inactivation of the antibiotic

-enhancing antimicrobial agent uptake by the bacteria

25
Q

give a specific example of the synergistic action of enhancing antimicrobial uptake by bacteria

A

penicillins (and other cell wall agents) increase the uptake of AMINOGLYCOSIDES by several bacteria like staphylococci, streptococci, enterococci, and Pseudomonas Aeruginosa

26
Q

give 3 general examples of antagonism

A

-static agents inhibit cidal activity

-induce enzymatic inactivation

-competing for the same activation/target site

27
Q

how is it that static agents can inhibit cidal activity and produce an antagonistic effect

A

cidals like bacteria that grow FAST - they target them the best

however, static agents slow the growth of bacteria

thus, cidal action is inhibited

28
Q

explain how 1 drug can induce enzymatic inactivation of another and exhibit an antagonistic effect

A

for example, if you give a beta lactam and then another drug that leads to the production of MORE BETA LACTAMASE - other drug will be broken down more

29
Q

explain what protein synthesis inhibitors cannot be used together and why

A

“MLS”

they all act on the same ribosome and will thus produce an antagonistic effect by competing for the same activation/target site

30
Q

explain what post antibiotic effect is and the formula to calculate it

give an example of an antibiotic that exhibits this

A

even when the drug is stopped, you still see its effects for a certain amount of time
vancomycin is a common example

PAE=T-C
(T = time for viability count to decrease 10 fold to the count before drug removal in the test culture)

C = time needed for viability count to go down 10 fold to an earlier count in the CONTROL culture

31
Q

we want 1 billion bacteria count. it takes 48 hours in the culture WITH VANCOMYCIN and 24 hours more when the drug is removed.

what is PAE

A

PAE = T-C

PAE = 24 hours

32
Q

name 3 general things that are contributing to resistance

A

evolution
clinical practices
environmental factors

33
Q

how can clinical practices contribute to resistance

A

giving wrong doses or a combination drug when only a single is needed (much more too)

34
Q

which particular bacteria is related to antibiotic use and antibiotic resistance

A

clostridios difficile

35
Q

simply explain how antibiotic resistance happens

A

there are a lot of bacteria and a few are drug resistane. antibiotics kill good and bad bacteria to fight the infection, but some bacteria with the resistance are NOT KILLED

they are allowed to grow and take over, and even give their drug resistance to other bacteria, causing more problems

36
Q

true or false

we can develop antibiotic resistance from animals

A

TRUE

animals get antibiotics and can develop resistance in their guts, and then if we eat that food when not cooked properly – we can get those same resistant bacteria

37
Q

a mechanism of drug resistance is by enhanced export of the antibiotic by the bacteria

how do they do this?

A

through efflux pumps

38
Q

a mechanism of resistance is by microbial enzyme release that destroys the antibiotic

give 2 examples of these enzymes

A

beta lactamases and acetyl transferases

39
Q

true or false

bacteria altering their microbial proteins is NOT a method of drug resistance

A

FALSE - it is

they can alter their TARGET PROTEINS, as well as their proteins that will transform antibiotic pro drugs into their active form

2 WAYS

40
Q

how can bacteria allow for REDUCED ENTRY of the antibiotic as a mechanism of resistance?

for which particular bacteria and antibiotics is this resistance mechanism important

A

mutations, decreases, or absences in PORIN CHANNELS in their outer membrane

important for gram negative bacteria and for antibiotics that have an INTRACELLULAR TARGET – there are less or no porins for them to get in

41
Q

which particular bacteria develops RND’s (resistance nodulation division exporters) as a mechanism of resistance?

A

pseudomonas

allows for efflux of the drug

42
Q

aside from RND (resistance nodulation division) exporters, name another transporter that bacteria can develop to allow for efflux of the antibiotic

what drug and gene encodes for it?

A

ATP binding cassette (APC) transporters

plasmodium falciparum multi drug resistance gene 1 (Pf mdr1)

43
Q

is it possible for bacteria to devlop alternative pathways to the pathway inhibited by the antibiotic as a way of developing resistance?

A

yes

44
Q

beta lactamases inactivate b lactam antibiotics by _______

A

hydrolysis

45
Q

aminoglycosides can be destroyed by bacteria by……

give specific example

A

being altered by acetylation, phosphorylation, or adenylation

cloramphenicol can be inactivated by chloramphenicol acetyltransferases

46
Q

explain the resistance mechanism of “incorporation of drug” and give an example

A

not only does the bacteria become resistant, but it can start to REQUIRE IT FOR GROWTH

for example, enterococcus easily develops vancomycin resistance and thus, after prolonged exposure, can develop strains that REQUIRE vancomycin for growth

47
Q

true or false

reduced affinity to the target site is a pretty rare mechanism of resistance

A

FALSE - used all the time

48
Q

bacteria can become resistance through modifying their antibacterial target

how do macrolides and tetracyclines do this??

A

by protecting their ribosomes

49
Q

bacteria can reduce affinity to their target site by acquiring a resistant form of the native, susceptible target

give a specific example

A

MRSA - caused by production of low affinity penicillin binding protein
(PBP -> PBP2a)
TARGET SLIGHTLY CHANGED

50
Q

How do bacteria targeted by fluoroquinolones mutate their natural target to develop resistance

A

modifying topoisomerase2

51
Q

can bacteria develop resistance through point mutations

A

YES

through point mutations in either the target or the activating enzymes

52
Q

in sulfonamide resistance, resistant strains overproduce _______ as a form of altering their metabolic pathway

A

overproduce PABA

53
Q

how can bacteria alter their metabolic pathway to develop resistance to vancomycin

A

produce D-Ala-D-lactate instead of D-Ala-A-Ala)

reduces affinity for vancomycin and vancomycin binding decreases

54
Q

TRUE OR FALSE*

the overexpression of porin channels is NOT a method to antibiotic resistance

A

TRUE!

this is a way for the AB to get in.

increased porin channels would allow for better antibiotic action

55
Q

true or false

overexpression of the drug target is a mechanism of antibiotic resistance

A

true

altering PBP to PBP2a

56
Q

true or false

plasma encoded beta lactamases are not a method of antibiotic resistance

A

FALSE - it is

57
Q

are efflux pumps good for resistance

A

YES

throws the drug out

58
Q
A

D&D Infectious Disease Midterm (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions