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IAHI Block 2 > 4 - Antibiotics 2 > Flashcards

4 - Antibiotics 2 Flashcards

1
Q

What is the action of vancomycin?

A

Vanc is a glycopeptide that inhitbits PG synthesis by physically binding to D-ala-D-ala on the PG precursor and preventing penicillin binding proteins from recognizing them as their substrate.

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2
Q

What are glycopeptides and what is their mechanism of action? What type of bacteria are they effective on?

A

Glycosylated, non-cyclic non-ribosomally synthesized peptide antibiotics (bactericidal).

Bind to Dala-Dala at the end of the peptide side chain in PG precursors, blocking penicillin binding proteins from recognizing them as their substrate. (This inhibits PG synthesis. )

Effective on gram + , NOT effective on gram - due to OM.

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3
Q

What mechanism do vancomycin-resistant bacteria use for resistance? What bacteria are associated with this?

A

Modification: acquire gene encoding machinery to produce altered PG structure that lacks D-ala-D-ala and contain D-ala-D-lac instead so Vancomycin is unable to bind to these precursors.

These genes can easily be transferred. And vanc resistance is associated with enterococci in hospital settings.

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4
Q

What is cycloserine and what is its mechanism of action? What is it often used to treat?

A

Inhibits PG by competitively inhibiting D-alanine in 2 sequential reactions involving alanine racemase and D-alanyl-D-alanine synthetase.

Higher affinity for enzyme than D-alanine.

Structurally similar to D-alanine and used in 2nd line treatment for TB

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5
Q

What is bacitracin? What is its mechanism of action? How is it used?

A

Peptide antibiotic that binds to pyrophosphate on the lipid carrier for PG precursors (bactoprenol-PP) and blocks its recycling.

Without a lipid carrieor, PG synthesis cannot continue.

Used topically b/c it’s toxic systemically.

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6
Q

What antibiotics work by targeting the cell envelope? What types of bacteria does each work on?

A

Daptomycin: gram +

Polymyxins such as polymixin B and colistin: gram -

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7
Q

What is the mechanism of action of daptomycin?

A

It’s a bactericidal, narrow spectrum lipopeptide that works on gram-positives.

Binds and disrupts cytoplasmic membrane, possibly via loss of membrane potential. Confers activity against antibiotic-resistant bacteria.

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8
Q

What is the mechanism of action of polymixins such as polymixin B and colistin?

A

It’s a bactericidal, narrow spectrum lipopeptide that works on gram-negatives.

Binds to LPS in OM of gram - bacteria, leading to disruption of the OM and cytoplasmic membrane. Confers activity against antibiotic resistant gram -s.

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9
Q

Describe protein synthesis (translation) in bacteria?

A

Protein synthesis occurs in 2 phases, initiation and elongation.

30S forms an initiation complex with mRNA message and initiator tRNA.

50S subunit joins in the functional 70S that forms peptide bonds to make proteins.

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10
Q

What are the names of some tetracyclines?

A

Tetracycline, doxycycline, and minocycline.

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11
Q

What is the mechanism of action of tetracyclines such as tetracycline, doxycycline, and minocycline?

A

BacterioSTATIC, broad spectrum (now limited due to resistance).

Bind to 30S subunit and interferes with binding of animoacyl tRNA to complex.

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12
Q

What are two mechanisms of resistance to tetracycline?

A

Tetracycline efflux pump: most common and provide resistance to all tetracycline-fam ABx

Mutations on ribosome: modifies the antibiotic target

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13
Q

What is the function of Tigecycline? What sets this apart from the tetracyclines?

A

MAde from modified minocycline.

BacterioSTATIC

Same action as tetracycline: binds 30S and interferes with aminoacyl tRNA binding to ribosomes.

Does NOT exhibis cross-resistance with tetracyclines.

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14
Q

What are the names of the aminoglycosides? Are they bactericidal or bacteriostatic?

A

Gentamicin, amikacin, tobramycin

They are the only bactericidal ribosomal inhibitors.

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15
Q

What is the mechanism of action of aminoglycosides such as gentamicin, amikacin, and tobramycin?

A

Bind irreversibly to 30S subunit to stop initiation of protein synthesis, causing premature release of mRNA from ribosome and causes misreading by translating ribosomes.

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16
Q

What is the mechanism of resistance to aminoglycosides such as gentamicin, amikacin, and tobramycin?

A

Enzymatic modification of the antibiotic: transferases catalyze addition of adenyl, acetyl, or phosphoryl group to prevent aminoglycoside binding to the ribosome.

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17
Q

What are the names of the macrolides? What type of antibiotic are they and what type of bacteria do they work on?

A

Erythromycine, azithromycin, and clarithromycin.

Bacteriostate and primarily work on gram-positive bacteria. (don’t cross OM of gram negatives)

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18
Q

What is the mechanism of action of macrolides such as Erythromycine, azithromycin, and clarithromycin?

A

Bind 502 ribosome subunit to block elongation of proteins.

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19
Q

What are the two mechanisms of resistance of macrolides such as Erythromycine, azithromycin, and clarithromycin?

A
  1. Methylation of ribosomal RNA: erythromycin can’t bind methylated ribosome.
  2. Efflux pump: can expel macrolides from cells and enable protein synthesis to continue
20
Q

What is the mechanism of action of Clindamycin? What is it used to treat?

A

Bacteriostatic; binds 50s subunit to block elongation.

Doesn’t work on gram negative; often used for treatment of community acquired MRSA, less so for hospital acquired MRSA.

Often used to treat infections by toxin-producing S. aureas but can cause C. diff colitis.

21
Q

What is the mechanism of resistance to clindamycin? What types of bacteria are resistant to this?

A

Methylation of rRNA so clindamycin can’t bind to the methylated ribosome.

Exhibits cross-resistance with macrolides - ie bacteria resistant to macrolides due to the presence of an erm gene are also resistant to clindamycin

22
Q

What is the mechanism of action of chloramphenicol? what are some side effects?

A

Bacteriostatic; broad-spectrum.

Toxicity due to lack of specificity limits use to very specific infections such as typhoid fever and rocky mt spotted fever.

Binds 50S ribosome to inhibit peptidyl transferase activity (elongation)

23
Q

What is the mechanism of resistance to chloramphenicol? How do bacteria become resistant?

A

Bacterial enzyme (chloramphenicol acetyltransferase; CAT) catalyzes addition of acetyl group to the drug, preventing ribosome binding by the drug.

Typically plasmid-borne.

24
Q

What is the mechanism of action of linezolid? What bacteria is it not affective on?

A

Binds unique site on 50S subunit (23S rRNA) preventing formation of 70S initiation complex.

Bacteriostatic, orally bioavailable. Narrow spectrum, not affective against more gram - or anaerobes.

25
Q

Describe the resistance associated with linezolid? Does cross-resistance occur with other ribosome targeting antibiotics?

A

It occurred rapidly after it was introduced.

Point mutations in ribosomal rRNA prevent linezolid binding (modification of antibiotic target)

No cross-resistance occurs due to its binding at a unique site.

26
Q

What is the mechanism of action of Nalidixic acid, a synthetic quinolone? What problems are associated with it?

A

Binds to bacterial DNA gyrase and/or topoisomerase to inhibits its function and disrupt DNA replication and repair. Causes DNA damage.

Narrow anti microbial spectrum; rapid selection for resistant mutants.

27
Q

What are some clinically useful quinolones? Describe their usefulness?

A

Fluoroquinolones such as norfloxacin, ciprofloxacin, moxifloxacin, and levofloxacin.

Bactericidial with broad spectrum.

All quinolones act by binding DNA gyrase or topoisomerase.

28
Q

What are the two mechanisms of action of resistance for quinolones?

A
  1. Point mutations in bacterial DNA gyrase that prevent antibiotic binding
  2. Efflux pump-mediated and altered porin resistance
29
Q

What is metronidazole used to treat? What is it’s mechanism of action? Is it bactericidal or bacteriostatic?

A

Anaerobic bacterial infections, common treatment for C diff pseudomembranous colitis.

In an anaerobic environment, bacteria reduce the nitro group to make a radical species, a toxic metabolite that damages DNA.

Bactericidal.

30
Q

What is the mechanism of resistance to metronidazole?

A

Alterations in metabolic pathways that cause bacteria to lose ability to reduce the nitro group.

31
Q

What is the mechanism of action of rifampin (rafampicin)? Is it bactericidal or bacteriostatic? What problem is associated with this drug?

A

Bactericidal.

Binds B subunit of bacterial RNA polymerase to inhibit polymerase activity and thereby presents RNA synthesis.

Problem: rapid selection for resistant mutants

32
Q

What is the mechanism of resistance to rifampin?

A

Acquisition of mutations in B subunit of RNA polymerase that prevents antibiotic from binding.

33
Q

What is the mechanism of action of Fidaxomicin? Is it bactericidal or bacteriostatic? What is the mechanism of resistance?

A

Bactericidal

Action: Noncompetitive inhibitor of RNA synthesis by binding to bacterial RNA pol.

Resistance: Acquisition of mutations in B subunit of RNA pol that prevent antibiotic from binding.

34
Q

What are anti-folates?

A

Metabolic analogs similar to metabolic intermediates and act the same way as competitive inhibitors to block the normal biosynthetic pathway.

35
Q

What is tetrahydrofolate?

A

A donor of a single carbon group for production of key biosynthetic precursors for nucleotide production.

Required for bacterial growth.

36
Q

What are two sulfonamides? What is their function?

A

Sulfamethoxazole and sulfadiazine.

Metabolic analogs of p-aminobenzoic acid that competitively inhibit dihydropteroic acid synthesis in the tetrahydrofolate pathway.

37
Q

What is trimethoprim?

A

A metabolic analog of dihydrofolate that competitively inhibits dihydrofolate reductase in the tetrahydrofolate biosynthetic pathway.

38
Q

What is the mechanism of resistance of anti-folates?

A

Acquisition of another gene encoding dihydrofolate reductase (usually plasmid-borne)

Mutations in the gene encoding dihydrofolate reductase.

39
Q

In what cases should a physician consider treating a patient with more than one antibiotic?

A
  1. Undetermined pathogen causing life-threatening infections need “coverage” for all likely pathogens (bacterial meningitis)
  2. Polymicrobial infection cause by bacteria with different susceptibility
  3. To avoid emergence of resistant mutants during long-term abx therapy (anti-TB course lasts 6-9 mo)
  4. Synergy: combined action of 2 drugs greater than sum of individual drugs
40
Q

What is synergism?

A

Combination of 2 agents results in at least 4-fold reduction in the minimum inhibitory concentration of antibiotic (amt needed to kill bacteria); or a combination that is more than additive.

41
Q

What are three examples of synergy?

A
  1. Two drugs act sequentially to block a metabolic pathway: sulfonamides and trimethoprim block steps in folic acid synthesis to have a bactericidal synergistic effefcts.
  2. One drug enhances uptake of another: penicilins (vanco) enhances uptake of aminoglycosides.
  3. One drug prevents inactivated or another: clavulanic acid inactivates B lactamases to prevent the cleavage of B-lactam abx to preserve their effectiveness.
42
Q

Besides synergism, what else can occur when combining antibiotics?

A

Antagonism: where the combination is less than the sum of the parts.

This can occur with some static and cidal combos, especially when the static is given first because cidal drugs work best on growing organisms and static drugs stop growth.

43
Q

What is a prime example of antagonism with antibiotic combinations?

A

Combining B-lactams can be antagonistic: 1st gen B lactams such as ampicillin, cephalosporins, cefoxitin, and imipenem strongly induce AmpC B-lactamases that can degrade many penicillins and 2nd and 3rd generation cephalosporins.

44
Q

Other than synergism and antagonism, what else can occur when combining two antibiotics?

A

Indifference: when two agents don’t work any better or worse than a single agent.

45
Q

What are biofilms?

A

bacteria growing in a multicellular aggregate on a surface; likely responsible for chronic infections like endocarditis and otitis media.

Bacteria in them exhibit enhanced tolerace to abx (NOT due to encoded resistance byt due to non-growing state and difficulty in abx penetration)

IAHI Block 2 (16 decks)

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