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
Q

why should u take the entire dosage of the drug for the right time?

A

because this will diminish the selection for mutations that can lead to low drug level resistance bc not all pathogens are eliminated

26
Q

goal of drug research

A

-short term higher dose antimicrobials that are effective and less expensive with less side effects

27
Q

possible long term solution to resistance

A

adding antimicrobials to animal feed worldwide

28
Q

assay for drugs that are commonly resistant

A

Kirby Bower disk diffusion test
-will test for resistance

29
Q

dilution test

A

minimum inhibitory concentration test to show the smallest concentration of drug that will VISIBLY inhibit growth

30
Q

MIC

A

minimum inhibitory concentration
-smallest amount to stop microbe growth
-goal: clear tube

31
Q

therapeutic index

A

ratio of the dose of the drug that is toxic to humans compared to its minimum effective dose

32
Q

what type of index is desired

A

high index

33
Q

drug resistant strain found in eye drops

A

P aeruginosa
-this is NOT all around us

34
Q

listeria monocytogenes

A

-gram positive
-doesnt form spores
-short (cocobacilli) or long filaments
-form flagella out of the body (1-4)
-no capsules

35
Q

what is listeria monocytogens resistant to?

A

heat, cold, salt, ph, bile

36
Q

where is listeria monocytogens found

A

in the fridge
-it is a psychotroph

37
Q
A