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My Notes > Antimicrobials: protein synth inhibitors > Flashcards

Antimicrobials: protein synth inhibitors Flashcards

1
Q

Which drug blocks the P site, thus preventing initiation of translation (occurs in the 30S subunit)?

A

Aminoglycosides

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1
Q

Which drug blocks the A site, thus prevents elongation of proteins (in 30S subunit)?

A

Tetracyclines

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1
Q

Which drug blocks the formation of a peptide bond, preventing linking of AAs on tRNA in the A site with the AA chain (or formyl methionine) in the P site? What enzyme is inhibited? Which subunit is involved?

A

Chloramphenicol; peptidyl transferase; 50S subunit

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1
Q

Which drugs block translocation? Which subunit is involved?

A

Macrolides and clindamycin; 50S subunit

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1
Q

Which drugs interfere with termination of translation?

A

None

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1
Q

Which drugs, like tetracyclines, inhibit A-site tRNA binding, but do so from the 50S subunit rather than the 30S side?

A

Dalfopristin/ quinupristin

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1
Q

What is the only -cidal protein synthesis inhibitor? Why?

A

Aminoglycosides, because it is a large molecule that fills the P site, causing kinking of the mRNA → induces frameshift in reading of sequence at the A site → lethal accumulation of abnormal proteins

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1
Q

What drug, like aminoglycosides, prevent formation of the initiation complex, but from the 50S side?

A

Linezolid

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1
Q

What drugs are used for VRSA and VRE?

A

Protein synthesis inhibitors:

  • Linezolid
  • Dalfopristin/quinupristin (as a back up)
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1
Q

What subunit is peptidyl transferase a part of?

A

50S

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1
Q

How do aminoglycosides get inside cells?

A

O2 dependent uptake mechanism → anaerobes are innately resistant

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1
Q

Which bugs can we use aminoglycosides for?

A
  1. G- aerobic rods: pseudomonas; TB, F. tularensis, Y. pestis (streptomycin)
  2. G+: enterococci
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1
Q

What kind of molecules are aminoglycosides? How does this relate to it’s elimination route and toxicity?

A

Sugars - H2O sol → eliminated by kidney
Toxicity: nephrotoxic, need to adjust dose in renal patients
Other toxicities: ototoxicity, NM blockade (neomycin)

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1
Q

What is unique about amingoglycosides compared with other protein synthesis inhibitors? How does this relate to dosing strategy?

A

-cidal, so instead of maintaining a steady state dose, we just need single large doses (you don’t have to keep shooting at a dead bacteria, but you might shoot again the next day in case any more are left); once daily dosing has dropped the incidence of side effects significantly

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1
Q

How do aminoglycosides cause NM blockade? What exotoxin is this similar to?

A

Prevents ACh release, like botulism toxin

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1
Q

What antibiotics are in triple antibiotic ointment? Which of these is associated most strongly with contact dermatitis?

A

It’s Neosporin, so think:

  1. Neomycin → contact dermatitis
  2. Polymyxin
  3. Bacitracin
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2
Q

How do bacteria resist aminoglycosides before being killed by them?

A

production of conjugating enzyme → fast elimination so it doesn’t have time to interfere with protein synthesis

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2
Q

Which protein synthesis inhibitors have largely replaced tetracyclines?

A

macrolides

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2
Q

What is the drug of choice in lyme disease?

A

doxycycline

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2
Q

What sort of bugs are tetracyclines especially good for?

A

Intracellular organisms like Rickettsia (eg. lyme) and Chlamydia because it accumulates intracellularly

2
Q

What is the key difference b/w doxycycline and minocycline? How does this contribute to their indications?

A

Doxy is lipid soluble → intracellular bugs

Mino is water soluble → bugs involved in gingivitis

2
Q

Which bugs is the tetracycline demeclocycline used for?

A

None- it blocks ADH receptors → would casue nephrogenic DI → used for SIADH

2
Q

What is the primary toxicity of tetracyclines?

A

they are chelators that bind most strongly to cations →

  1. decreased absorption of these ions in the gut
  2. when the drugs are absorbed they bind strongly to bones, which inactivates the drug, causes discoloration of enamel (avoid use in children), and would ↓ bone formation if used in pregnancy (also teratogenic)
2
Q

Who should never be prescribed tetracyclines?

A

children and pregnant women

2
Q

When is minocycline used? What is its main side effect?

A

in dentistry for gingivitis; can cause vestibular (balance) dysfunction

2
Q

What is the primary mode of resistance to tetracyclines?

A

plasmin-encoded transport pumps

2
Q

What is the significance of “phen” in drug names (eg. acetaminophen, chloramphenicol)?

A

indicates a phenyl group is present → lipid soluble → processed in liver and crosses BBB, no renal tox.

2
Q

What are the uses for chloramphenicol?

A

Very wide spectrum of use b/c lipid sol and good distribution to brain – used for meningtitis

2
Q

What is the mechanism of chloramphenicol?

A

inhibits peptidyl transferase in the 50S subunit → blocks peptide bond formation

2
Q

How is chloramphenicol processed? Why is this significant when treating infants?

A

in liver via conjugation; infants don’t have UDP-glucuronyl transferase so they can’t process the drug

2
Q

What are the main side effects of chloramphenicol?

A
  1. BM suppression (dose-dependent = hypersensitivity, not aplastic anemia)
  2. Gray baby syndrome
  3. Inhibits P450 → drug interactions
3
Q

Why do infants get gray baby syndrome if given chloramphenicol?

A

because they are deficient in UDP-glucuronyl transferase: 1. they can’t process the drug → ↑ [ ]
2. displacement of bilirubin from binding sites → kernicterus (bilirubin-induced brain damage, primarily occurs in infants)

3
Q

what suffix = macrolide?

A

-thromycin

3
Q

What do macrolides work on?

A
  1. G+ cocci (staph [not MRSA-need vanc], strep)
  2. THE drugs for atypical organisms (chlamydia, mycoplasma, LEGIONELLA, MAI)
  3. UTI - ureaplasma
3
Q

What is special about azithromycin compared with other macrolides?

A

most H2O soluble →

  1. the only macrolide that doesn’t inhibit p450
  2. the safest macrolide in pregnant women
3
Q

Why are macrolides often given as a surgery prophylaxis?

A
  1. they kill lots of GI bugs

2. they activate motilin receptors → ↑ motility after anaesthesia

3
Q

What are some concerns with high doses of macrolides?

A
  1. reversible deafness (ototoxic)

2. GI distress (kills flora and promotes motility)

3
Q

What drug is important for macrolide-resistant strep. pneumoniae? What group is this drug in?

A

Telithromycin; ketolide

3
Q

What is the primary mode of resistance against macrolides?

A

methylation of 23S rRNA-binding site prevents binding of drug to 50S unit

3
Q

What is the mechanism of action of macrolides and clindamycin?

A

block translocation

3
Q

What do we use clindamycin for?

A

Narrow spectrum:

  1. G+ (incl. S. aureus)
  2. Anaerobic flora (B. fragilis)
3
Q

Where does clindamycin love to accumulate? How does this relate to one of the uses for clindamycin?

A

in bone → tx for S. aureus osteomyelitis (not useful for salmonella or pseudomonas osteomyelitis seen in sickle cell and IVDU patients - use quinolones for these G- bugs)

3
Q

How is clindamycin used in the treatment of anaerobes?

A

mostly in aspiration pneumonia where there are anaerobes where there is mixed aerobic/anaerobic flora

3
Q

What was the first drug known to cause pseudomembranous colitis (C. Diff overgrowth)?

A

clindamycin

3
Q

Macrolides and clindamycin are identical in mechanism of action. What about in mechanism of resistance?

A

Same – both are inhibited by methylation of binding site on the 50S subunit

4
Q

Linezolid - what is it’s mechanism similar to? What is it used for?

A

aminoglycosides (prevents initiation complex formation), but for the 50S subunit.
Used for VRSA, and VRE

4
Q

What is the primary toxicity of Linezolid?

A

Bone marrow suppression, particularly platelets → severe bleeding

48
Q

What are the streptogramins? What are they used for? How do they work? What are the toxicities?

A

quinupristin/dalfopristin (always given together for synergy) - for VRSA and VRE; prevent A site tRNA binding (like tetracyclines); tox not worked out yet

My Notes (23 decks)

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