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IPFC 2 Midterm 1 > ID- Pharmacology > Flashcards

ID- Pharmacology Flashcards

1
Q

What is the MOA of B-lactam antibiotics

A
  • inhibits cell wall synthesis by binding covalently to the active sites of PBPs to inhibit the transpeptidation reaction
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2
Q

What does the absorption of penicillin depend on? Which can be given orally? With food? Without food?

A

Depends on acid stability

Oral: Penicillin V, amoxicillin, ampicillin & cloxacillin

Amox–> ONLY one to give with food
The rest without food

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3
Q

What is the most serious ADRs of penicillins? Explain its mechanism? Common side effects? dose-dependant?

A

Hypersensitivity
- Antigens are presented during penicillin metabolism when they are transiently bound to a protein –> results in hapten that is identified by non-self by the immune system

Common: uticaria, fever

Not dose-dependant

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4
Q

What is the primary mechanism of B-lactam resistance

A

B-lactam inactivation by B-lactamase

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5
Q

What are the B-lactam inhibitors?
MOA?

A

Clavulanic acid, sulbactam, tazobactam

MOA
- high affinity for catalytic site of B-lactamases –> inhibit hydrolysis of B-lactam

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6
Q

What does adding clavulanic acid to amoxicillin add to the spectrum?

A

Targets strains of STAPH. AUREUS and some gram-negative (better H. flu, better Proteus mirablis, + klebsiella pneumo)

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7
Q

What are the anti-staphylococcal penicillins?

A

Nafcillin, methicillin, cloxacillin

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8
Q

What are the anti-pseudonomal penicillins? what else does it target

A

ticarcillin, pippercillin
- targets gram-negative aerobes

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9
Q

What are some ADRs of cephalosporins

A

Sensitizing
Nephrotoxicity (at high doses)

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10
Q

What is the MOA of vancomycin?

A

Targets cell wall (not b-lactam)
- binds the Ala-Ala terminus of the peptidoglycan pentapeptide (instead of PBP)

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11
Q

How to administer vancomycin

A

IV
- oral for GI infections

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12
Q

Main Spectra of vancomycin

A

only gram-pos

  • does not penetrate outer membrane of gram-negative bacteria
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13
Q

What are serious toxicities with vancomycin?

A
  • in ear and kidney
  • increase the risk of aminoglycoside nephrotoxicity
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14
Q

What is the resistance associated with vancomycin? Innate and acquired?

A

Innate (natural): to gram-neg

Acquired:
- altered cell wall precursors by switching the 2nd Ala group to lactate or serine
- binds less vancomycin

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15
Q

Fosfomycin MOA?

A

non b-lactam cell wall agent
-1. PEP analog –> inhibits MurA enzyme (needed for peptidoglycan cell wall synthesis)
2. Decrease the ability of bacteria to interact with the urinary tract epithelium

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16
Q

What are the protein synthesis inhibitors of bacteria? (4)

A
  • Aminoglycosides
  • Tetracyclines
  • Macrolides and clindamycin
  • linezolid
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17
Q

Which ribosomes do bacteria use for protein synthesis? Which do mammals?

A

30S + 50S

mammals: 40S + 60S

18
Q

What is the MOA of tetracyclines?

A

bind to 30S subunit and block binding of incoming tRNA
- results in non-functional proteins and wrong AA addition

19
Q

What is the metabolism of tetracycline?

A

Excreted into urine, bile, some enterohepatic recycling

20
Q

What are the ADRs of tetracyclines

A

Gi
photosensitization
Liver toxicity (large doses)
Renal toxicity

21
Q

What are toxicities of tetracyclines? exception?

A

calcium chelation (related to dose)
- tetracyclines bind to and damage growing bones and teeth

Exception: doxycyclines

22
Q

What is the primary resistance mechanism of tetracyclines

A

Drug efflux pumps

23
Q

Explain what each efflux pumps work in?
Tet AE
Tet K
Tet M

A

Tet AE: in gram-neg bacteria
Tet K: in staphlyococci against tetracyclines
Tet M: in gram positive

24
Q

Which tetracycline is less susceptible to efflux pumps? why? Exception

A

Tigercycline
- bc of bulky side chain

except Proteus bacteria + pseudomonas

25
Q

What are the macrolides (3)

A

erythromycin
clarithromycin
azithromycin

26
Q

What is the MOA of macrolides

A

bind reversibly to the 50S ribosomal subunit
- inhibits transpeptidation/translocation steps in protein information

27
Q

What are PK notes for each
erythromycin
clarithromycin
azithromycin

A

erythromycin: must be enteric coated
clarithromycin: best absorbed
azithromycin: empty stomach

28
Q

What is the order of half-lives of macrolides

A

Azith > clarithromycin > erythromycin

29
Q

Explain the resistance that macrolides experience (4)

A
  1. Reduced permeability of cell membrane (in gram neg)
  2. Active efflux (in gram-pos)
  3. Esterases production –> hydrolyze macrolides
  4. Target modification of 50S
30
Q

What is the MOA of clindamycin

A

Same as macrolide
(bind reversibly to the 50S ribosomal subunit
- inhibits transpeptidation/translocation steps in protein information)

31
Q

What is the resistance of clindamycin? What is the difference between this and macrolides

A
  • Reduced permeability of cell membrane (gram-neg)
  • Target modification of 50S

NOT AFFECTED BY EFFLUX PUMP (gram-pos)

32
Q

What are the DNA-targeted antibiotics? (3)

A
  • Fluroquinolone
  • sulfonamide
  • Trimethorprim
33
Q

What are the bactericidal fluoroquinolones and respiratory fluoroquinolones?

A

Bactericidal
- cipro
- norfloxacin
- ofloxacin

Respiratory
- levofloxacin
- gemifloxacin
- moxifloxacin

34
Q

What is the MOA of fluoroquinolones

A

Block DNA synthesis by inhibiting 2 bacterial enzymes

  1. Topoisomerase II
    - prevents relaxation of DNA so that normal transcription/translation does not occur
  2. Topoisomerase IV
    - prevents separation of replicated chromosomes into daughter cells
35
Q

What is the unique toxicity associated with fluoroquinolones

A

Cartilage damage (not recommended for patients under 18)

36
Q

What are the resistance mechanisms of fluoroquinolones? (3)

A
  1. Target enzyme mutation (gyrA subunit of Topoisomerase II)
  2. Change in permeability
  3. Proteins that protect from Topoisomerase II
37
Q

What is the MOA of metronidazole?

A

The nitro group on metronidazole is reduced –> highly reactive nitro radical anion –> affects DNA

  • O2 inhibits metronidazole
    (made for anaerobes)
38
Q

What is metronidazole toxicity associated with? reason?

A

Associated with duration of therapy

39
Q

What are resistance notes of metronidazole?

A
  • Mutations that impair the production of nitro radical anion
  • Decreased oxygen-scavenging (increase O2 in the cells = bad)
40
Q

What is fidoxamicin used against?

A

macrolytic antibiotic against gram-positive and anaerobic bacteria
- used for C. difficile infections

Oral

41
Q

MOA of fidoxamicin?

A

Binds the sigma subunit of RNA polymerase
- more selective for bacteria

42
Q

What is the MOA of oeltamivir/zanamivir?

A

Neuraminidase inhibitors
- interact with neuraminidase and causes a conformational change; this inhibits the enzyme’s activity
- results in the virus aggregating at the cell surface and reduced spread

IPFC 2 Midterm 1 (8 decks)

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