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Phase 2 Block 1 > Antibiotics (1-3) > Flashcards

Antibiotics (1-3) Flashcards

1
Q

What 4 things must happen for an antibiotic to work?

A

Bind to target site(s) in the bacteria
Occupy the right number of binding site in a bacteria
Remain at the binding site for enough of the metabolic process that the bacteria is inhibited
Antibiotic must get to the right site of action

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2
Q

There are 2 ways that antibiotics can impact the cell wall on bacteria

A

Inhibition of cell wall synthesis (β-lactams, vanco)
Alteration of cell membrane function (daptomycin)
These antibiotic work outside the nucleus

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3
Q

There are 3 ways that antibiotic can impact the function of bacteria to exert their effect (work inside the cell)

A

Inhibition of protein synthesis
Inhibition of nucleic acid synthesis
Alteration of cell metabolism

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4
Q

What groups of antibiotic inhibit protein synthesis?

A

Macorlides
Tertracyclines
Aminioglycosides
Linezolids
Clindamycin

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5
Q

What groups of antibiotic inhibit nucleic acid synthesis?

A

Fluroquinolones

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6
Q

What groups of antibiotic alter cell metabolism?

A

Sulphonamides
Trimethoprim

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7
Q

What is the breakpoint in context of minimum inhibitory concentration (MIC)?

A

For each organism-antibiotic pair there is a cut-off MIC that defines susceptibility - this is the breakpoint

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8
Q

Are antibiotic equally effective in IC pts as immunocompetent pts?

A

No; antibiotic work with the immune system to produce their effect
This makes it important to take into account the pts immune system when selecting antibiotic and its dosing

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9
Q

What is the difference between bacteriostatic and bactericidal antibiotic?

A

Antibiotic that are bacteriostatic will inhibit rather than kill
Antibiotic that are bactericidal will kill
However, bacteriostatic antibiotic can become bactericidal at concentrations that exceed their MIC

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10
Q

What are the 4 mechanisms of resistance bacteria can use to avoid being killed by antibiotic?

A

Enzymatic destruction
Modified cell wall porins (antibiotic cant get in)
Efflux pumps (antibiotic gets pumped out)
Altered binding sites (antibiotic cant attach where it needs to)

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11
Q

From slide 15 and on questions are based on tick marks
Go back and add more questions if context needed

A
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12
Q

How do β-lactams work?

A

Bind to penicillin binding proteins (PBPs) and interfere with formation of the peptidoglycan barrier —> cell wall dysfunction and cell death
- β-lactams bind to many different PBPs

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13
Q

What are the most common mechanisms of bacterial resistance to β-lactams?

A

Enzymatic destruction via β-lactamases
Alteration of PBP sites

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14
Q

What is the most common adverse drug reaction associated with β-lactams (esp penicillin and cephalosporins)?

A

Hypersensitivity reactions, type 2 more than type 1 and others

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15
Q

Of the oral penicillins which one absorbed well orally?

A

Amoxicillin

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16
Q

Which cephalosporins have poor oral absorption?

A

Cefuroxime
Cefixime

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17
Q

Which β-lactams must be taken on an empty stomach?

A

Pen V
Cloxacillin

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18
Q

Cloxacillin is effective against strep spp. (mostly) but not against one type of staph aureus. Which one is it and why?

A

MRSA
This type of staph aureus has developed resistances to β-lactams as it had developed or acquired the ability to make β-lactamase

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19
Q

What staph spp. are susceptible to cloxacillin?

A

MSSA are susceptible; the only one not susceptible is MRSA

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20
Q

How can susceptibility to β-lactams be restored in bacteria?

A

Using β-lactamase inhibitors (ex. Clavulanate and tazobactam)
Using this these drugs with β-lactams —> better gram (-) susceptibility and is very effective vs bacteria that make only β-lactamase

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21
Q

What can cloxacillin do that amoxicillin cant and vice versa?

A
22
Q

Why are gram (-) susceptible to amoxicillin and not cloxacillin?

A
23
Q

Why is there probably no point to adding a β-lactamse inhibitor to cloxacillin?

A
24
Q

This IV antibiotic has a longer side chain allowing it to bind to different PBPs —> better gram (-) susceptibility. It is the most comprehensive penicillin to date

A

Pipercillin/tazobactam
Between the long side chain and the presence of tazobactam (β-lactamase inhibitor) it gives very strong coverage for gram (-) bacteria inc those that make β-lactamase

25
Q

Why are β-lactam/β -lactamase inhibits not used against ESBL producing bacteria?

A
26
Q

What is the main advantage of pipercillin/tazobactam compared to other antibiotic for gram (-) so far?

A

This might be a repeat but maybe keep?

27
Q

What 2 ares did cephosporins improve on from penicillins?

A

Better stability against β-lactamses by some gram (+) and gram (-)
Improved on activity agasint gram (-) organisms

28
Q

What aspect of coverage improves as you move along the generations of cephalosporins?

A

Ability to cover gram (-) organisms but you may lose some S. aureus susceptibility

29
Q

1st gen celphalosporins have good coverage against these 3 gram (-) bacteria

A

Proteus spp.
E. Coli
Klebsiella spp.

30
Q

2nd gen celphalosporins have better coverage than 1st gen for these 4 gram (-) bacteria

A

H. Influenzae
Proteus spp.
E. Coli
Klebsiella spp.

31
Q

Which cephalosporin is most like amoxicillin/clavulanate?

A
32
Q

Cephalexin is probably a better choice of an antibiotic over cefuroxime in what situation?

A
33
Q

Why have none of the β-lactams been ineffective agasint M. pneumoniae?

A
34
Q

This was the first cephalosporin that was effective against p. aeruginosa. It also has poor activity agasint gram (+) bacteria.

A

Ceftazidime

35
Q

What does pipercillin/tazobactam have in common with ceftazidime with regards to microbial susceptibility?

A
36
Q

Which bacteria (in general) will pipercillin/tazobactam work against that ceftazidime will not?

A
37
Q

Why does cefixime having activity agsint N. Meningitidis not really that useful?

A
38
Q

Why is ceftobiprole effective against MRSA and cloxacillin is not?

A
39
Q

What coverage problem did carbapenems solve that penicillins and cephalosporins couldn’t cover?

A

Works against serious anaerobes like b. fragilis

40
Q

What β-lactam(s) is piptaz most like form an antimicrobial susceptibility perspective?

A
41
Q

What is the one of the adverse effects that we see with imipenem that is not as common with other β-lactams?

A
42
Q

What final problem were macrolides able to solve that weren’t covered with β-lactams, cephalosporins, and carbapenems?

A

They also work against cell wall deficient organisms

43
Q

Which macrolide is the worst for causing stomach upset?

A

Erythromycin

44
Q

Tetracyclines are similar in MoA and spectrum to which class of antibiotic?

A

Macrolides

45
Q

What is a something to consider when taking tetracycline by mouth?

A

Should not be taking with foods rich in multivalent cations (Al, Ca, Fe, Mg, Zn)
Up to 20% of drug can bind these molecules when taken with foods rich in these molecules
Avoid taking with milk

46
Q

Dose adjustments are needed for this tetracycline based on renal function

A

Doxycycline

47
Q

How do quinolones work?

A
  • Block bacterial DNA synth by inhibiting bacterial topoisomerase II and topoisomerase IV
  • Topoisomerase IV important to gram (+), topoisomerase II more important to gram (-)
48
Q

What is a notable adverse effect of fluoroquinolones?

A

Can affect sugars (+ or -) esp in diabetics

49
Q

Aminoglycosides exhibit a significant post-box effect of 6hrs. What is the importance of this?

A

They are dosed once a day as serum level below the MIC is still capable of killing the organism with these antibiotic

50
Q

These are very important ADRs to look for when giving TMP-SMX

A

Common presentation of sulfa exposure — morbilliform or maculopapular rash
Rare for cross reactivity with other sulphonamides
Monitor for SJS, TENs, and DRESS (all rare)
↑ in serum Cr (competes with tubular secretion of Cr)
↑ K (blocks tubular secretion of K)
↓ Na
Possible teratogenicity and increased risk of kernicterus in newborn

Phase 2 Block 1 (15 decks)

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