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Micro Cards > 8.13_Antibiotics > Flashcards

8.13_Antibiotics Flashcards

1
Q

4 types of antibacterials

A

cell wall synthesis, protein synthesis, dna synthesis, membrane structure

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2
Q

Minimum inhibitory concentration (bacteriostatic)

A

minimum concentration where antibiotics start to inhibit the growth of the microbes, this is typically visible to the eye in colony growth, usually much lower concentration that cidal for same antibiotic so it just prevents growth

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3
Q

Minimum bactericidal concentration (bactericidal)

A

minimum concentration at which the bacteria all start to die, you typically need bacterial growth for this to work, usually a similar concentration for cidal compared to static so just go ahead and kill

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4
Q

Disk diffusion

A

test for susceptibility to antibiotics, add disk of drug around colony of bug and if bug grows right up to disk then it is not susceptible, but if circle around disk then you know it is. Can measure size of circle to determine susceptibility

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5
Q

E-Test

A

Have a strip with different concentrations of drugs, along the strip bacteria do or do not grow. There is a point where growth begins and this could be your bactericidal or bacteriostatic concentration

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6
Q

Molecular techniques for bacterial resistance

A

Sequencing and PCR can show us if well known resistant mutations are present in a bacteria

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7
Q

Pharmacodynamics

A

This is the effect of the drug on the body, like time course and intensity of therapeutic

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8
Q

Pharmacokinetics

A

The body’s effect on the drug, absorption distribution metabolism

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9
Q

Cmax and AUC in Pharmacodynamics

A

Cmax is peak conc of the drug, AUC is area under the curve which is how long the drug stays above the minimum concentration

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10
Q

Time Dependent Killing versus Concentration Dependent Killing

A

Time means you want to maximize time above the critical concentration so you make a wider curve whereas concentration means you want to make that concentration high so have a more vertical curve

Examples of TDK is penicillin and cephalosporins
Examples of CDK is Fluoroquinolones and aminoglycosides

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11
Q

Post antibiotic affect

A

time it takes the bacteria to return to log phase of growth following a dosage of antibiotics, longer PAE means less often dosing, gram + have longer PAE than –

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12
Q

B-lactams

A

class of antibiotics that interfere with the bacterial cell envelope, they have a beta lactam ring that highly resembles the DalaDala part of the peptide linkage in peptidoglycan, so transpeptidase will confuse the two and actually incorporate a B-lactam which disrupts the enzyme activity

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13
Q

5 classes of B-lactams

A

Penicillins, cephalosporins, monobactams, clavams, Carabapenems, these all have slightly different structure in their B lactam ring

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14
Q

B-lactams modes of Resistance

A

B lactamase can enzymatically inhibit the drug by cleaving the B lactam ring

Can alter the drug target by changing the DalaDala sequence, this often occurs through horizontal gene transfer

Alter drug exposure by using pumps to increase the efflux of drugs out of the cell, this is mainly in G— that this occurs

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15
Q

Extended Spectrum B-lactamases

Metal Dependent B-lactamase (NDM-1)

A

ESBLs are able to work against all classes of b-lactams

NDM-1 is just another important and new lactamase

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16
Q

Clavulanic Acid

A

this is a B-lactamase inhibitor, so can inhibit the inhibitor of the b-lactams

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17
Q

PBPs or penicillin binding proteins

A

transpeptidase binds penicillin instead of DalaDala, hence the name, for resistance sometimes these can have super low affinities for B-lactams but still be an active transpeptidase

This arises through mutation or horizontal transmission

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18
Q

Altered penicillin transport

A

2 modes of resistance here for gram negative bacteria

1 is that there can be decreased membrane permeability to the drug and the 2nd is that a bacteria can inherit a mutation that alters efflux of pumps and can pump more antibiotic out

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19
Q

Glycopeptides

A

These are still under the group of antibiotics that target the synthesis of the cellular envelope, but they target the transglycosylation not the transpeptidase like B-lactams

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20
Q

Vancomycin

A

Best example of a glycopeptide as it targets the transglycosylase of the peptidoglycan layer, the mechanism is that it covers the DalaDala which is the end of the peptide strand meaning the transglycosylase cannot recognize and add the next sugar

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21
Q

Vancomycin resistance modes

A

Not an enzyme known to inhibit the action of glycopeptides, DalaDala isnt directly encoded by gene so you cannot get a mutation that changes that, and it is used for gram + mainly so no altered drug uptake like seen in gram–

The only mode of resistance is changing the DalaDala to DalaDlac which means the vancomycin wont recognize the peptide change and the transglycosylase can work

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22
Q

Bacitracin

A

inhibits regeneration of peptidoglycan lipid carrier, often used in topical infections like skin ointment

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23
Q

Phosphomycin

A

prevents NAG from attaching to NAM and peptide in peptidoglycan

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24
Q

Cycloserine

A

prevent NAM to peptide attachment

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25
Q

Isoniazid

A

used for mycobacterium by inhibiting the synthesis of mycolic acid

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26
Q

Ethambutol

A

inhibits the arabinotransferases which make the network of arabinogalactans in mycobacterium

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27
Q

two antibiotics for mycobacterium

A

isoniazid and ethambutol

28
Q

Lipopeptides

A

permeate the not so dense PG layer in gram +, but cannot enter through outer membrane of gram -, these form pores in the cytoplasmic membrane by binding phosphatidylglycerol which is mainly just in prokaryotic membranes

important to note the lung surfactant of our lungs does have the phosphatidylglycerol so never use for pneumoniae treatment

29
Q

Daptomycin

A

example of a lipopeptide

30
Q

Folate

A

often synthesized in prokaryotes in the process of making DNA, RNA and proteins, therefore this process can be a target of antibiotic

31
Q

sulfonamides and trimethoprim

A

sulfonamides target an upstream enzyme in folate synthesis and trimethoprim targets a more downstream action, hitting with both of these makes resistance much less likely

32
Q

sulfonamides

A

bacteriostatic, go against g+ and –, an example is sulfamethoxazole

33
Q

resistance to sulfonamides

A

can have a change to the enzyme targeted, can swamp the system with folate precursor, and can decrease the uptake of sulfonamides

34
Q

synergistic, additive, and antagonistic combination therapy

A

synergistic means they work together, additive just means not much change in the two and antagonist means drug fight each other

35
Q

trimethoprim

A

bactericidal, used in combo with a sulfonamide which is a synergistic combo, it targets DHFR

36
Q

Quinolones/fluoroquinolones

A

bactericidal and g- better than g+, inhibit DNA synthesis in prokaryotes by inhibiting DNA gyrase which is a topoisomerase that is different from human topos, now 4 generations of these drugs with new generations improving g+

EXAMPLE is ciprofloxacin, this drug has side effect of tendon rupture and cardiac issues

37
Q

Topoisomerase II versus IV with fluoroquinolones

A

topo II is inhibited and DNA cannot be replicated
topo IV is inhibited and DNA replicated but the two circular strands cannot be unattached from each other as they are linked like a chain

38
Q

resistance to quinolones

A

Mutations in gyraseA and topoisomerase genes can lead to an altered drug target that the drug no longer recognizes, in gram - may have porin proteins to alter drug uptake, or increased efflux due to mutations increasing their activity,

Also can have cross resistance between quinolones and other antibiotics and host derived antimicrobial factors…multidrug resistance

39
Q

Rifamycins

A

bactericidal or bacteriostatic depending on concentration, inhibits mRNA synthesis, mainly used against mycobacterium tuberculosis or meningococal prophylaxis

Mechanism is it binds to DNA dependent RNA poly better in pros than euks

40
Q

Rifampin

A

Best example of a rifamycin that inhibits mRNA synthesis

41
Q

resistance to rifamycins

A

Easy to evolve, so rifamycins rarely used in monotherapy, arises from mutations in genes coding for RNA polymerase

42
Q

Nitroimidazoles

A

produce free radicals in DNA and ruin it, bactericidal and is against ANAEROBES!, they are prodrugs meaning they must be converted to active once inside bacterial cell

43
Q

Metronidazole

A

Example of a nitroimidazole that ruins DNA with free radicals

44
Q

Nitroimidazole resistance

A

mainly in mutations causing there to be no activation of the drug once it is in the bacterial cell

45
Q

30s ribosomal protein inhibitors

A

Aminoglycosides and tetracyclines

46
Q

50s ribosomal protein inhibitors

A

Chloramphenicol, macrolides, lincosamides, streptogramins, oxazolidinones

47
Q

Aminoglycosides

A

bind 30s subunit, bactericidal, gram-rods, some of these can also work against mycobacterium, anaerobic bacteria are intrinsically resistant, enter gram - cells by messing with the LPS in outer membrane

48
Q

streptomycin, gentamicin

A

examples of aminoglycosides that bind the 30s subunit and are bactericidal against gram - rods and some mycobacteria

49
Q

Aminoglycosides resistance

A

can enzymatically inactivate the drug, can change drug target of small subunit of ribosome through mutation, and can decrease uptake and increas efflux
Since all three scenarions of resistance can occur, resistance is very common in aminoglycosides

50
Q

Aminoglycoside and B-lactam combination therapy

A

used together so the b-lactam can break up the gram+ layer of PG and poke some holes in outer membrane, this allows the aminoglycoside to now enter the cell and bind ribosome subunits

51
Q

Tetracyclines

A

bind 30s unit, are bacteriostatic, active versus G+/-, mycoplasma, and intracellular bacteria that have accumulated inside human cells

cations inhibit so no milk in digestive and inhibits bone growth so not good for pregnancies

52
Q

tetracycline, and doxycycline

A

two examples of tetracyclines that bind the 30s unit of ribosomes

53
Q

Tetracyclines resistance

A

a ton of efflux pumps, and can alter drug target with ribosome protection proteins that displace drug from ribosome

54
Q

Chloramphenicol

A

binds 50s unit, bacteriostatic usually, but cidal against capsulated organisms, work against +/-

55
Q

Chloramphenicol resistance

A

Enzymatically inactivate the drug with acetyl transferases

56
Q

Macrolides

A

bind 50s unit, bacteriostatic, mainly G+ but can do G- like Chlamydia

57
Q

Erithromycin and azithromycin

A

examples of macrolides, bind 50s unit and bacteriostatic

58
Q

Lincosamides

A

bind 50s unit, work on g+/- anaerobes!!! it is highly associated with c. difficile associated colitis

59
Q

Clindamycin

A

examples of lincosamide, binds 50s unit and works on +/- anaerobes

60
Q

Streptogramins A and B

A

used in combo because as individuals are bacteriostatic but together they are bactericidal, SA interferes with peptide bond formation and SB interferes with ribosome after it is used and is looking for a new mRNA, so sorta targets two points in a ribosome cycle so if ti misses one it can still get it

61
Q

MLSb resistance

A

resistance to macrolides, lincosamides, and streptogrammins B due to similar mechanisms, the bacteria methylate the ribosomes so the antibiotics cannot act on it

It also can inducibly make bacteria resistand to clindamycin

62
Q

D test

A

Used to check if MLSb is inducibly causing clindaycin resistance, see the D shape between obvious resistance to macrolide or ERY and then clindamycin shows more susceptibility on side farthest from ERY, means ERY is inducing resistance to clindamycin

63
Q

Oxazolidinones

A

bind to 23s of 50s, bacteriostatic, against g+ that are commonly resistant to other antibiotics,

64
Q

Oxazolidinones resistance

A

no cross resistance in these, only resistance is mutations in 23s rRNA gene

65
Q

Linezolid

A

example of an oxazolidinones that bind the 23s of the 50s

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