L1 Antibacterial drugs I Flashcards

1
Q

Why are antibiotics important for modern medicine

A

modern medicine is often invasive and calls for good control over bacterial infections

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2
Q

What is chemotherapy

A

using chemicals to aim a certain disease or pathogen

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3
Q

What is arsanilic acid (atoxyl)

A

It is an antibiotic used against syphilis

It was later chemically optimized into neosalvarsan which is less toxic and more specific to the bacteria

(syphilis was later treated with penicillin)

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4
Q

What are the 4 targets of antibiotics when it comes to gram-negative and gram-positive bacteria (4)

A
  1. DNA inhibitors: sulfonamides, trimethoprim, quinolones, nitrofurans
  2. Cell membrane disruptors: polymyxins, daptomycin
  3. Protein synthesis inhibitors: aminoglycosides, tetracyclines
  4. Cell wall synthesis inhibitors: beta-lactams, vancomycin
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5
Q

What is the difference between bacteriostatic and bactericidal

A

bacteriostatic: inhibits cell division
-immunocompetent host
-non-life threatening, uncomplicated infection

bactericidal: actively kills bacterial cells
-deep-seated infections (endocarditis, meningitis); heart, brain
-where the immune system has a harder time accessing
-life threatening

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6
Q

What is CFU (colony-forming units)

A

It measures the number of live bacteria in a sample

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7
Q

TF: there are 2 types of antibiotics; bactericidal or bacteriostatic

A

False, some antibiotics can be both depending on the context

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8
Q

What is MIC (minimal inhibitory concentration)

A

It is the the minimum amount of antibiotic required to inhibit bacterial growth/division

it is used to find out weather the antibiotic is working or if the bacteria is resistant

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9
Q

What is the MBC (minimal bactericidal concentration)

A

It is the minimum amount of antibiotic required to kill (all) bacteria

This is done by plating the dilution test samples on an agar plate that does not have any antibiotics

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10
Q

What is the susceptibility assay

A

It is to test weather a bacteria is susceptible to an antibiotic

This is done by adding drug-impregnated disks onto an agar plate swabbed with a given bacteria - then incubated. Greater nongrowth diameters indicate greater susceptibility

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11
Q

TF: MIC and MBC are considered susceptibility assays

A

True, they are a part of susceptibility testing

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12
Q

In which cases are broad spectrum antibiotics used

A

when the causative agent cannot rapidly be identified

e.g. tetracyclines, fluoroquinolones, carbapenems

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13
Q

Why is the irresponsible use of broad spectrum antibiotics dangerous

A

it disturbs the microbiota and may promote antimicrobial resistance

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13
Q

Why are narrow spectrum antibiotics beneficial in contrast to broad spectrum antibiotics

A

-it does not target the microbiome
-broad spectrum can confer resistance in bacteria due to selective pressure

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13
Q

In which cases are broad spectrum antibiotics used?

A

when the clinical cause is known

e.g. penicillins, monobactams

daptomycin is very narrow, developed due to MRSA

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14
Q

What are the 3 kinds of antimicrobial therapies

A
  1. Definitive drug therapy: ideal scenario where antimicrobial agent is selected based on the organism identified and its susceptibility
  2. Empiric therapy: initial approach where antibiotic selection is guided by clinical presentation and knowledge of most common causative agents (cannot wait for susceptibility assay)
  3. Prophylactic drug therapy: use of antimicrobial agent to prevent infection
15
Q

Why are aminoglycosides combined with penicillin? What is this an example of?

A

aminoglycosides require penicillin’s ability to inhibit the cell wall in order to reach their target (ribosomes) and take action

This is an example of synergy

15
Q

What are the 3 possibilities when combining antimicrobial agents

A
  1. synergy
  2. indifference
  3. antagonism
  • synergy can be additive or potentiating
16
Q

Provide an example of antibacterial synergy (that is not aminoglycosides + penicillin)

A

sulfonamides + trimethoprim: both block folate synthesis but at different pathways

17
Q

How can bacteria develop resistance so quickly

A

They divide at a high rate i.e. very fast, thus increasing the possibility of resistance developping

18
Q

What are the 7 major mechanisms of bacterial resistance?

A
  1. active efflux of drug via efflux pump
  2. target protection via protein blocking the active site of target
  3. inactivation of antibiotic via enzyme
  4. decreased influx (via porins for example)
  5. target site modification
  6. target bypass (bacteria makes new pathways to achieve the same metabolic functions inhibited by the drug)
  7. Downregulation (of porins for example)
19
Q

How do bacteria gain resistance via gene exchange? (3)

A
  1. plasmid exchange (bacterial conjugation)
  2. transduction with virus (bacteriophage)
  3. uptake of free DNA from environment