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Pharm Block 3 > Antibacterials > Flashcards

Antibacterials Flashcards

1
Q

What are the types of cell wall agents?

A

beta-lactams, Vancomycin, Telavancin, Fosfomycin, Bacitracin*

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2
Q

What are the types of cell membrane agents?

A

Polymyxins, Cyclic Lipopetides

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3
Q

What are the types of nucleic acid agents?

A

Quinolones, Nitrofurans, Rifampin, Fidaxomicin, Metronidazole*

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4
Q

What are the types of proteins synthesis agents?

A

Aminoglycosides, Spectinomycin, Tetracyclines, Tigecycline, Chloamphenicol, Macolides, Clindamycin, Linezolid

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5
Q

What are the types of anti-folates?

A

Sulfonamides, Trimethoprim*

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6
Q

General properties of beta-lactams

A

usually bactericidal
effective against gram pos and neg
most effective against actively growing bacteria

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7
Q

Mechanism of action of beta-lactams

A

Inhibit transpeptidases by binding to PBP, which catalyze cell wall cross links
competitive, irreversible

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8
Q

What are the methods of bacterial resistance to beta-lactams

A
  • beta-lactamases
  • altered PBP
  • beta-lactam agent can’t reach PBP
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9
Q

What types of killers are beta-lactams

A

time-dependent

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10
Q

Examples of beta-lacatamase inhibitors

A

clavulanic acid, tazobactam

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11
Q

What is an example of a beta-lactam and some of its derivatives(?)

A
  • Penicillin
    • amoxicillin, ampicillin, Penicillin V, Penicillin G, piperacillin, ticarcillin, oxacillin*
  • Cephaolosporin
    • 1st gen: cefazolin, cephalexin
    • 2nd gen: cefuroxime, cefoxitin
    • 3rd gen: ceftriaxone, ceftazidime
    • 4th gen: cefepime*
  • Imipenem*
  • Azteronam*
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12
Q

What is special about oxacillin*

A

It is resistant to Staphylcoccal beta-lacatamase

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13
Q

Excretion/metabolism of penicillins

A 
~30% hepatic metabolism
mostly renal (20% glomerular filtration/80% tubular anionic excretion)
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14
Q

Adverse reactions of penicillins

A
  • allergic
    • anaphylaxis
    • rash
  • diarrhea, enterocolitis
  • elevated liver enzymes
  • hemolytic anemia
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15
Q

What is the mechanism of action of Vancomycin*

A
  • bactericidal
  • inhibits cell wall synthesis by binding to free carboxyl end (D-ala-D-ala) of the pentapeptide to interfere with transpeptidation and transglycosylation
  • could also disrupt cell membranes and inhibit RNA synthesis
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16
Q

When and how are vancomycin* used

A
  • IV for systemic infections
  • oral for C. diff enterocolitis
  • bactericidal
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17
Q

Excretion/metabolism for vancomycin*

A

active form excreted via glomerular filtration

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18
Q

Adverse reactions to vancomycin*

A
  • “red neck” syndrome
  • nephrotoxicity
  • phlebitis
  • ototoxicity
  • hypersensitivity, skin rashes, neutropenia
  • “pain and spasm” syndrome
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19
Q

Mechanism of action of Fosfomycin*

A

inhibits synthesis of peptidoglycan building blocks by inactivating enolpyuvyl transerase, an early-stage cell wall synthesis enzyme

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20
Q

What are Fosfomycin* used for

A

uncomplicated UTI caused by E. Coli enterococcus

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21
Q

Fosfomycin* toxicity

A

headache, diarrhea, nausea, vaginitis

22
Q

Bacitracin* mechanism of action

A

interferes w/ cell wall synthesis by interfering with lipid carrier that exports early cell wall components through the cell membrane

23
Q

How are bacitracin* used

A

topical only, because very nephrotoxic against gram-positive cocci and bacilli

24
Q

Toxicity of bacitracin*

A

allergic dermatitis

25
Q

Polymyxins mechanism of action

A

act as cationic detergents that bind LPS in the outer membrane of gram-negatives

26
Q

An example of a polymyxin and how it’s used

A
  • Polymyxin B*
    • topically, esp for Pseudomonas and other gram-negative infections
    • systemic use has potential for serious nephro and neuro toxicity
27
Q

An example of a cyclic lipopeptides and its mechanism of action

A
  • Daptomycin*

- binds to bacterial cytoplasmic membrane, causing rapid membrane depolarization

28
Q

Side effects of Daptomycin*

A

nausea, diarrhea, GI flora alteration, muscle pain and weakness

29
Q

Mechanism of action of Quinolones

A

Inhibit DNA gyrase (usually alpha subunit) to interfere with control of bacterial DNA winding

30
Q

Type of killing by Quinolones

A
  • Bactericidal

- dependent on AUC24hr/MIC

31
Q

How is resistance to Quinolones achieved

A
  • altered DNA gyrase

- combination of decreased permeability

32
Q

What are the two kinds of quinolones

A

fluorinated and nonfluorinated

33
Q

What are non fluorinated quinolones effective against

A

Enterobacteriaceae in urinary tract

34
Q

What are examples of fluorinated quinolones

A

norfloxacin, ciprofloxacin, moxifloxacin*

35
Q

Which quinolines are used for urinary tract infection?

A

norfloxacin, ciprofloxacin

36
Q

What are some adverse reactions of quinolones

A

nausea, vomiting, abd pain, enterocolitis, peripheral neuropathy

37
Q

How is the distribution of quinolines?

A

well-distributed, including the CSF

38
Q

MAO of nitrofurans

A

nitroreductase converts them to reactive compounds which can damage DNA

39
Q

Which nitrofuran is used for UTI

A

nitrofurantoin*

40
Q

What are the uses for nitrofurans?

A

UTI and intestinal infections

41
Q

Adverse reactions of nitrofurans

A

nausea, vomiting, diarrhea

42
Q

MAO of rifampin*

A

inhibits bacterial RNA synthesis by binding RNA polymerase beta

43
Q

What is rifampin* used for

A
  • primarily for pulmonary tuberculosis

- also used for prophylaxis for meningococcal meningitis and Haemophilus influenza type b meningitis

44
Q

Adverse reactions to rifampin*

A
  • serious hepatotoxicity (<1%)
  • induces hepatic enzymes (many CYPs) that inactivate other drugs
  • orange color (urine, saliva, tears, sweat)
45
Q

MAO of Fidaxomicin*

A

nonceompetitive inhibitor of RNA polymerase, which inhibits RNA synthesis

46
Q

What is Fidaxomicin* used for

A

C. difficile infection (third line to metronidazole, vancomycin)

47
Q

Excretion/metabolism of Fidaxomicin*

A

fecal elimination, some metabolism by intestinal cells

48
Q

Adverse reaction of Fidaxomicin*

A

GI upset (4-10%), GI bleeding (4%), neutropenia (2%)

49
Q

MAO of Metronidazole*

A

Multiple steps:

  1. anaerobes reduce the nitro group of metronidazole*
  2. resulting product disrupts DNA and inhibits nucleic acid synthesis
50
Q

How does resistance to Metronidazole* occur

A

anaerobes lose ability to reduce nitro group of metronidazole*

Pharm Block 3 (10 decks)

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