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Foundations Exam 3 > Antibiotics Against DNA/Protein Synthesis > Flashcards

Antibiotics Against DNA/Protein Synthesis Flashcards

1
Q

name 5 classes of antibiotics that are cell wall synthesis inhibitors

A
  1. penicillins
  2. cephalosporins
  3. carbapenems
  4. monobactams
  5. glycopeptides
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2
Q

name 2 classes of antibiotics that are cell membrane disrupters

A
  1. polymyxins
  2. daptomycin
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3
Q

what class of antibiotic is an inhibitor of DNA replication (DNA gyrase and topoisomerase IV inhibitors)

A

fluoroquinolone

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4
Q

what are 2 classes of antibiotics that are inhibitors of DNA biosynthesis (folate metabolism inhibitors)

A
  1. sulfonamides
  2. trimethoprim
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5
Q

what 4 classes of antibiotics are protein synthesis (50S) inhibitors

A
  1. macrolides
  2. lincosamide
  3. oxazolidinones
  4. pleurmutilin
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6
Q

what 2 classes of antibiotics are protein synthesis (30S) inhibitors?

A
  1. aminoglycosides
  2. tetracyclines
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7
Q

what class of antibiotics are Gentamicin, Tobramycin, Streptomycin, Amikacin, Neomycin, Paromomycin, and Plazomicin?

A

aminoglycosides: inhibitors of bacterial 30S ribosomal subunit (protein synthesis inhibitors)

*note that Streptomycin and Amikacin are both 2nd-line anti-Mtb drugs

[also remember that tetracyclines also inhibit 30S]

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8
Q

what class of antibiotics are Doxycycline, Minocycline, Eravacycline, and Tigecycline?

A

tetracyclines: inhibitors of bacterial 30S ribosomal subunit (protein synthesis inhibitors)

[remember that aminoglycosides are also 30S inhibitors]

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9
Q

what is the basic mechanism of aminoglycosides (Gentamicin, Tobramycin)?

A

target 16S rRNA A-site of 30S subunit and irreversibility interfere with protein synthesis in 3 ways!

  1. block initiation
  2. block translocation (—> premature termination)
  3. cause mRNA misreading

bactericidal (vs most protein synthesis inhibitors which are bacteriostatic)

exhibit post-antibiotic effect: antibacterial activity persists after drug clearing - allows for once-daily dosing

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10
Q

explain why aminoglycosides (Gentamicin, Tobramycin) are able to be administered with once-daily dosing, despite being cleared from the body before the next dose

A

aminoglycosides: inhibit 16S rRNA A-site of 30S ribosomal subunit by blocking initiation, blocking translocation, and causing mRNA misreading

exhibit post-antibiotic effect: antibacterial activity persists after drug clearing - allows for once-daily dosing

*note that aminoglycosides are bactericidal (unlike most protein synthesis inhibitors which are bacteriostatic)

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11
Q

of the aminoglycosides (30S subunit inhibitors), Tobramycin, Gentamicin, and Amikacin are similar in that they are all used for…

A

most frequently prescribed for systemic treatment, via IM or IV (drugs are basic amines - bad oral bioavailability)

serious infections by aerobic Gram(-) bacilli - mainly used as second agents for empiric therapy for septicemia, complicated UTIs, nosocomial resp. tract infections, osteomyelitis, intra-abdominal infections, etc

however, use is limited because there are less toxic agents available

[do NOT work well against anaerobes]

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12
Q

which 3 aminoglycosides (30S inhibitors) are most frequently prescribed for systemic treatment, as second agents for empiric therapy for serious infections caused by aerobic Gram(-) bacilli?

what class of drugs are they typically given in combination with to prevent emergence of resistance?

A

Tobramycin, Gentamicin, Amikacin

typically given with beta-lactam antibiotics (synergistic)

*note that use is limited because there are less toxic agents available

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13
Q

how is bacterial resistance to aminoglycosides (30S inhibitors) typically conferred, and which aminoglycoside is resistant to this?

A

resistance to aminoglycosides is typically through gene expression that produces enzymes which modify aminoglycosides

Amikacin is resistant to these enzymes (recall this is an anti-TB drug)

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14
Q

which aminoglycoside (30S inhibitors) is used as a 2nd-line agent against TB, and a first-line agent against tularemia and plague?

A

Streptomycin: 2nd-line agent in combination for TB, first-line mono-therapeutic option for tularemia and plauge

recall that tularemia is caused by Francisella tularensis and plague is caused by Yersinia pestis

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15
Q

Neomycin, Paromomycin, and Plazomicin are all aminoglycosides (inhibit 30S subunit) - what are their respective clinical uses?

A

Neomycin: topical infections (toxic!) - part of Neosporin

Paromomycin: intraintestinal Amebiasis, taken orally even though basic because infection is in GI tract itself

Plazomicin: complicated UTIs, including pyelonephritis

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16
Q

which aminoglycoside (30S inhibitor) is restricted to topical use because it is very toxic?

A

Neomycin (part of Neosporin!)

*note that topical includes skin and eyes (eye drops)

fun fact: recall that Bacitracin, antibiotic against lipid phosphatase in peptidoglycan synthesis, is also in Neosporin! (triple antibiotic)

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17
Q

explain why it makes sense that Paromomycin, an aminoglycoside (30S inhibitor) can be taken orally, despite its basicity?

A

basic drugs are not absorbed well, usually given via IV or IM (not oral)

however, Paromomycin is mainly used for treatment of intraintestinal amebic infection, so it can be given orally because the infection is right there in the GI tract!

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18
Q

which aminoglycoside (30S inhibitor) is relatively new and approved for complicated UTIs, including pyelonephritis?

A

Plazomicin

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19
Q

what are the 2 primary adverse reactions associated with aminoglycosides (30S inhibitors)?

A
  1. nephrotoxicity: metabolized entirely by kidney and accumulate at high levels - major limiting factor of widespread use and length of use
    *esp. Neomycin (!), Tobramycin, Gentamicin
  2. ototoxicity: also limits length of use - auditory (tinnitus) or vestibular (vertigo, ataxia) damage; note these effects tend to be irreversible
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20
Q

how do tetracyclines function to inhibit the bacterial 30S ribosomal subunit?

what kind of bacteria does this work on?

A

bind to 30S subunit and prevent aminoacyl-tRNA binding to the A site, thereby preventing peptide elongation

bacteriostatic for aerobic and anaerobic Gram+/- bacteria (broad spectrum)

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21
Q

aminoglycosides and tetracyclines are 2 classes of antibodies that both inhibit the bacterial 30S ribosomal subunit, thus preventing protein synthesis

describe the differences in their mechanism, differences in type of bacteria they are effective against, and state which is bactericidal vs bacteriostatic

A

aminoglycosides: target 16S rRNA A-site of 30S subunit and irreversibly inhibit protein synthesis via 3 ways - block initiation, block translocation, cause mRNA misreading
bactericidal with postantibiotic effect, mostly aerobic Gram(-)

tetracyclines: bind 30S subunit and prevent aminoacyl-tRNA binding to A site, blocking peptide elongation
bacteriostatic and broad spectrum

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22
Q

explain why tetracyclines (30S inhibitors) should not be taken with dairy products or antacids

A

tetracyclines chelate (= bind metal) multivalent cations, such as Ca2+, Mg2+, Fe2+, and Al3+, which are found in products such as dairy or antacids

absorption form the gut following oral administration is therefore impaired by these cations and byproducts that contain them

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23
Q

You’re prescribing Doxycycline, a tetracycline (30S inhibitor) to your patient. As you’re advising them on proper medication adherence, you make sure to tell them to avoid this food product…

explain why

A

avoid dairy and antacids (among other things) when taking tetracyclines

tetracyclines chelate (bind) multivalent cations (calcium, magnesium, iron, aluminum)

absorption from the gut following oral administration is impaired by these cations and byproducts containing them

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24
Q

which tetracycline (30S inhibitors) must be administered by IV? what is it used for?

A

Tigecycline: really a glycylcycline, poorly absorbed orally but has longer half-life than other tetracyclines

reserved for treatment of refractory infections caused by multi-drug resistant bacteria, including Vancomycin-resistant enterococci (VRE) and Methicillin-resistant Staph. aureus (MRSA)

25
Q

Doxycycline is the most heavily prescribed tetracycline (30S inhibitor), and it is the first line of treatment for these 3 illnesses:

bonus if you can name the other 2 things it’s typically used for (but not first line for)

A
  1. Rickettsial infection (Rocky Mountain spotted fever, typhus, Q fever)
  2. Chlamydial STIs (male urethritis, female cervicitis)
  3. early localized Lyme disease with erythema migrans (EM, bull’s eye rash)
  4. community-acquired bacterial pneumonia (for empiric therapy, in combination with amoxicillin)
  5. Acne Vulgaris (in conjunction with topical therapies)
26
Q

what is the first line antibiotic for:

  1. Rickettsial infection (Rocky Mountain spotted fever, typhus, Q fever)
  2. Chlamydial STIs (male urethritis, female cervicitis)
  3. early localized Lyme disease with erythema migrans (EM, bull’s eye rash)
A

Doxycycline: tetracycline (30S inhibitor)

also used for:
- community-acquired bacterial pneumonia (CABP) empiric therapy
- Acne Vulgaris in conjunction with topical therapies

27
Q

which tetracycline (30S inhibitor) is recently approved for complicated intra-abdominal infections?

A

Eravacycline

28
Q

what are 4 primary adverse reactions associated with tetracyclines (30S inhibitors)?

A
  1. GI upset
  2. deposition in newly-forming teeth/bones (children), due to chelation (binding metals - calcium) - CONTRAINDICATED for long use in children
  3. photosensitization (bad sunburns)
  4. hepatotoxic - CONTRAINDICATED during pregnancy
29
Q

which antibiotics are contraindicated for long use in children due to deposition in newly-forming teeth and bones? explain why

A

tetracyclines (30S inhibitors): chelate cations such as calcium (in bones and teeth)

can deposit in teeth, causing fluorescence/discoloration/enamel dysplasia

can deposit in bone, causing deformity or growth inhibition

30
Q

what class of antibiotics do Azithromycin, Clarithromycin, and Erythromycin belong to? what bacteria are they effective against?

A

Macrolides: inhibit bacterial 50S ribosomal subunit and inhibit translocation step of protein synthesis

bacteriostatic vs aerobic Gram+ and some Gram-

differences in clinical utility between drugs due to pharmacokinetic properties

31
Q

which type of macrolide (50S ribosomal inhibitor) has the longest half life?

A

Azithromycin - 3 day half-life, allows for less frequent dosing and shorter duration of treatment

32
Q

what 4 illnesses is Azithromycin (macrolide, inhibits 50S subunit) used for? bonus if you can indicate for which it is the preferred drug

A
  1. Bordetella pertussis (“whooping cough”): preferred drug
  2. community acquired bacteria pneumonia (CABP): preferred adjunctive option for empiric therapy in combination with amoxicillin
  3. chlamydial STIs: preferred in pregnant women who cannot tolerate hepatotoxicity of doxycycline (tetracycline)
  4. Streptococcal pharyngitis (“strep throat”): alternative for patients with beta-lactam allergy
33
Q

what is the drug of choice for treating Bordetella pertussis whooping cough?

A

Azithromycin: macrolide, targets bacterial ribosomal 50S subunit to inhibit translocation step

34
Q

Your patient is a pregnant woman with a chlamydial STI. What is the best drug to prescribe to them for their STI? explain your choice

A

usual first-line drug for chlamydial STI is doxycycline (tetracycline, targets 30S); however, tetracyclines are contraindicated during pregnancy due to hepatotoxicity

therefore, the drug of choice for this patient is Azithromycin (macrolide, targets 50S)

35
Q

what type of antibiotic is Erythromycin, and what is it a first-line treatment for?

A

Erythromycin: macrolide, targets 50S ribosomal subunit to inhibit translocation

*first-line drug for diphtheria caused by Corynebacterium diphtheriae

36
Q

what are the 4 primary adverse reactions of macrolides (50S inhibitors)?

A
  1. GI disturbance (esp. Erythromycin!!)

less common:
2. arrhythmias (cardiac)
3. allergic reactions
4. hepatotoxicity (probably hypersensitivity reaction)

37
Q

what is the mechanism and use of Clindamycin (lincosamide that targets 50S subunit)?

A

mechanism: blocks peptide transfer and ribosomal translocation

use: bacteriostatic vs aerobic and anaerobic Gram+/-

primarily treats anaerobic infections above the diaphragm (Bacteroides fragilis, Clostridium perfringens)

ex: aspiration pneumonia, lung abscess, oral infection

38
Q

why does it make sense that Clindamycin (lincosamide, targets 50S subunit) is commonly used to treat oral infections?

A

Clindamycin is especially effective against anaerobic Gram(-) bacteria, which heavily colonize the oral cavity

39
Q

what adverse effect of Clindamycin (lincosamide, 50S inhibitor) is the limiting factor of its use?

A

major disrupter of microbiome in GI tract

—> Clostridium difficile diarrhea (from overgrowth) and pseudomembranous colitis

[recall that C. diff is very hard to treat]

40
Q

what class of antibiotics do Linezolid and Tedizolid belong to? what is the mechanism of this class?

A

Oxazolidinones: inhibit bacterial 50S ribosomal subunit by binding to A-site of 23S rRNA, blocking initiation of protein synthesis

41
Q

what are Linezolid and Tedizolid (oxazolidinones, target 50S subunit) used for?

A

bacteriostatic vs aerobic Gram(+)

used for treating multi-drug resistant Gram+ bacteria, including MRSA and VRE (restricted to this use to prevent emergence of resistance)

42
Q

what are the most common adverse side effects of Linezolid and Tedizolid, oxazolidinones which target the 50S ribosomal subunit? (3)

A
  1. thrombocytopenia
  2. GI disturbance
  3. peripheral neuropathy
43
Q

what antibiotic does this describe?
- binds to A site of 23S rRNA to block initiation of protein synthesis
- bacteriostatic vs aerobic Gram+
- can treat MRSA and VRE
- side effects include thrombocytopenia

A

Linezolid or Tedizolid: oxazolidinones (inhibit 50S ribosomal subunit)

use restricted to treating multi-drug resistant Gram+ to preserve their effectiveness

side effects: thrombocytopenia, GI disturbance, peripheral neuropathy

44
Q

what is the mechanism of Lefamulin, a pleuromutilin?

A

Lefamulin: binds BOTH A and P sites of 23S rRNA, blocking peptidyl tRNA binding and ribosomal translocation (pleuromutilins inhibit 50S subunit)

mostly bactericidal with also some bacteriostatic activity (depends on the pathogen)

45
Q

what is Lefamulin (pleuromutilin, inhibits 50S subunit) used for?

A

mostly bactericidal with some bacteriostatic activity vs Gram+/- pathogens associated with respiratory tract infections

approved to treat community acquired bacterial pneumonia (CABP), or as alternative to patients who can’t tolerate beta-lactams or fluoroquinolones

46
Q

why is Lefamulin (pleuromutilin, inhibits 50S subunit) at risk for drug-drug interactions?

A

metabolized by CYP3A4 - drugs that modulate this enzyme would interfere with Lefamulin metabolism

47
Q

how do antifolates work to inhibit bacterial DNA synthesis?

A

inhibit synthesis of purine bases

ex: sulfonamides and trimethoprim-sulfonamide combinations

48
Q

what 2 antibiotics belong to the sulfonamide class, which are antifolates? how do they work?

A
  1. Sulfamethoxazole (SMX)
  2. Sulfisoxazole

sulfonamides are PABA analogs that competitively inhibit dihyropteroate synthase, which converts PABA to dihydrofolic acid (first step of pathway in purine synthesis)

sulfonamide-susceptible bacteria cannot use folate, must synthesize it from PABA (p-aminobenzoic acid)

[recall that sulfonamides are antifolates, which inhibit DNA synthesis by inhibiting synthesis of purine bases!]

49
Q

what are sulfonamides (Sulfamethoxazole/SMX and Sulfisoxazole) used for, and what are their adverse effects?

A

treat UTIs, but not as monotherapy (due to resistance)

sulfonamides are hyperallergenic

[remember that sulfonamides are PABA analogs in purine synthesis]

50
Q

how does trimethoprim (TMP), a type of anti-folate, work to inhibit DNA synthesis?

A

selectively inhibits bacterial dihydrofolate redactase (DHFR), the 2nd step in purine synthesis pathway

[sulfonamides like SMX compete with PABA in the first step, and in combination TMP-SMX is bactericidal!]

51
Q

what kind of drug is Bactrim?

A

TMP-SMX: combination of trimethoprim (TMP) and Sulfamethoxazole (SMX, a sulfonamide)

these are both under umbrella of antifolates (inhibit DNA synthesis)

SMX blocks first step of purine pathway (competitive with PABA), while TMP blocks second step (selectively inhibits bacterial dihydrofolate reductase)

alone they are both bacteriostatic but in combination they are bactericidal

[DO NOT confuse wirh Bacitracin, antibiotic against lipid phosphatase of peptidoglycan synthesis]

52
Q

name 3 illnesses for which TMP-SMX (antifolate) is a first-line drug

bonus if you can name for which it is a second-line option

A

TMP-SMX: trimethoprim + Sulfamethoxazole (Sulfonamide), blocks first 2 steps of purine synthesis pathway

first line:
1. uncomplicated UTIs (empiric)
2. Pneumocystis pneumonia (direct)
3. Shigellosis (direct)

2nd line: Salmonella

53
Q

if a patient takes TMP-SMX for more than 5 days, what should you become concerned for?

A

serious adverse effects including megaloblastic anemia and leukopenia

TMP-SMX: trimethoprim + Sulfamethoxazole (Sulfonamide), blocks first 2 steps of purine synthesis pathway

54
Q

what kind of antibiotics are fluoroquinolones (FQs), and what common ending do they all have in their names?

A

Fluoroquinolones (FQs): type of DNA gyrase/Topoisomerase IV inhibitors

all end in “-oxacin” !

ex: Ciprofloxacin, Ofloxacin, Enoxacin
and
respiratory FQs: Levofloxacin, Gemifloxacin, Moxifloxacin (recall these are 2nd-line TB drugs)

55
Q

what kind of antibiotics are Ciprofloxacin, Ofloxacin, and Enoxacin?

A

Fluoroquinolones (FQs): inhibit bacterial DNA gyrase/Top. IV

also respiratory FQs: Levofloxacin, Gemifloxacin, Moxifloxacin (recall these are 2nd-line TB drugs)

56
Q

the bacterial target of fluoroquinolones (end in “-oxacin”) is slightly different depending on whether bacteria is Gram(+/-)… specify

A

Gram(-): DNA gyrase is primary target

Gram(+): Topoisomerase IV is primary target

bactericidal against both!

57
Q

for which 3 illnesses are fluoroquinolones (inhibit DNA gyrase/Top. IV) first line drugs? bonus if you can name 2 illnesses they are alternatives for

A
  1. complicated UTIs, including pyelonephritis (Ciprofloxacin, Levofloxacin)
  2. Shigellosis and Salmonella (Ciprofloxacin, Levofloxacin)
  3. Anthrax prophylaxis (Ciprofloxacin)

also:
4. CABP (community acquired bacterial pneumonia) - respiratory FQs (Levofloxacin) are alternatives for patients who cannot tolerate beta-lactams
5. Otitis Externa (swimmer’s ear)

58
Q

in general, fluoroquinolones (DNA gyrase/Top IV inhibitors) are well tolerated or cause some GI disturbance

however, there are 2 more serious risks (though uncommon) - what are they?

A

neurological: delirium, hallucinations, seizures

cardiovascular: arrhythmias caused by QT prolongation

Foundations Exam 3 (28 decks)

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