chapter 11 pt 2 Flashcards

1
Q

aminoglycosides

A

interfere w proteins
-bind to 30s subunit so the mRNA gets misread cause frameshift
-inhibit protein synth
-useful for aerobic gram negativie robs and some gram positive bacteria

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2
Q

which microbes make aminoglycosides

A

streptomyces and micromonospora

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3
Q

tetracyclines

A

block protein synthesis by binding to 30S subunit and preventing aminoacyl trna from binding to mrna ribosome complex

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4
Q

chloramphenicol

A

blocks peptide bond formation and protein synthesis
-synthetic
-TOXIC

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5
Q

why is chloramphenicol toxic?

A

inhibits mitochondrial ribosomes

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6
Q

macrolides

A

erythromycin

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7
Q

erythromycin

A

goes to 50S subunit and prevents ribosome translocation so cant move onto mRNA

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8
Q

erythromycin drugs

A

-zithromax, azithromycin and z pack
-low toxicity and broad spectrum

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9
Q

fluoroquinolones

A

bind to DNA gyrase and topoisomerase IV so bacterial DNA cant replicate

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10
Q

fluoroquinolone drugs

A

-ciprofloxacin
-broad spectrum

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11
Q

why does fluoroquinolone use have to be monitored

A

because overuse can lead to ciprofloxacin resistant bacteria

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12
Q

what are most drugs that block metabolic pathways?

A

synthetic

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13
Q

what is the most important metabolic pathway blocker?

A

sulfonamides/ sulfa drugs

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14
Q

how do sulfas work

A

-competitive inhibition
-block enzyme needed for folic acid synthesis
-narrow spectrum
-bacteriostatic (stops growth no KILL)

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15
Q

golden age of antibiotics

A

1940 - 1980

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16
Q

antibiotic classes

A

penicillins, tetracyclines, macrolides, fluoroquinolones, carbapenems

17
Q

resistance

A

reduced effectiveness of antimicrobial drug

18
Q

how does resistance arise?

A

genetic versatility, an aquired mutation, intrinsic/ natural resistance mechanism that existed before it was exposed to the drug

19
Q

example of intrinsic natural resistance mechanism

A

a gram positive drug can’t affect a gram negativie drug

20
Q

where are spontaneous mutations coming from?

A

chromosome genes
-can transfer from species to species bc it comes from resistance factor int he plasmid that transposons

21
Q

natural selection

A

eventually the population will be resistant bc the non resistance cells are destroyed
-this does not happen until exposure to the drug occurs

22
Q

MRSE

A

methicillin resistant staphylococcus aureus
-resistant to many antibiotics
-most are skin infections in community

23
Q

MRSA in hospital

A

life threatening sepsis, pneumonia or surgical site infection

24
Q

steps to reduce drug resistance

A

-accurate diagnosis and drug
-compliance to correct dosage for the required time
-multidrug therapy

25
why should u take the entire dosage of the drug for the right time?
because this will diminish the selection for mutations that can lead to low drug level resistance bc not all pathogens are eliminated
26
goal of drug research
-short term higher dose antimicrobials that are effective and less expensive with less side effects
27
possible long term solution to resistance
adding antimicrobials to animal feed worldwide
28
assay for drugs that are commonly resistant
Kirby Bower disk diffusion test -will test for resistance
29
dilution test
minimum inhibitory concentration test to show the smallest concentration of drug that will VISIBLY inhibit growth
30
MIC
minimum inhibitory concentration -smallest amount to stop microbe growth -goal: clear tube
31
therapeutic index
ratio of the dose of the drug that is toxic to humans compared to its minimum effective dose
32
what type of index is desired
high index
33
drug resistant strain found in eye drops
P aeruginosa -this is NOT all around us
34
listeria monocytogenes
-gram positive -doesnt form spores -short (cocobacilli) or long filaments -form flagella out of the body (1-4) -no capsules
35
what is listeria monocytogens resistant to?
heat, cold, salt, ph, bile
36
where is listeria monocytogens found
in the fridge -it is a psychotroph
37