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PHAR221 > L18 Antibacterial drugs > Flashcards

L18 Antibacterial drugs Flashcards

1
Q

Bacterial cell wall structure simple desc

A

3-dimensional lattice comprising peptidoglycan

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2
Q

Glycan (aminosugar)

A
  • chains cross-linked by peptide linker chains
  • peptidase activity of penicillin binding proteins
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3
Q

What are the linear strands of two alternating aminosugars in a baceterial cell wall

A
  • N-acetyl-muramic acid (NAMA)
  • N-acetyl-glucosamine (NAG)
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4
Q

β-lactams

A

Interactions between β-lactam drugs and various penicillin binding proteins (PBPs) in bacteria explain differences in antibacterial specificity

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5
Q

β-lactams is a

A

Cell wall synthesis inhibitors and is essential for antibacterial activity

Lactam is a drug class

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6
Q

Amoxicillin (natural or semisynthetic)

A

Semisynthetic

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7
Q

Amoxicillin (broad or narrow)

A

Broad

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8
Q

Amoxicillin - β-lactamase resistant?

A

no

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9
Q

Clavulanic acid (natural or semisynthetic)

A

Semisynthetic

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10
Q

Clavulanic acid (broad or narrow)

A

-

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11
Q

Clavulanic acid- β-lactamase resistant?

A

β-lactamase inhibitor

Yes

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12
Q

A penicillin-like antibiotics

A

Amoxicillin

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13
Q

A beta-lactamase inhibitor drug

A

Clavulanic acid

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14
Q

How does Clavulanic acid work

A

It works by preventing bacteria from destroying amoxicillin so rendering them effective against beta-lactamase producing bacteria.

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15
Q

Pharmacokinetics of penicillins

A
  • stability in acid varies
  • lipid insoluble
  • do not enter mammalian cells
  • cross the blood–brain barrier only if the meninges are inflamed
  • most penicillins are eliminated via the renal route (90% by tubular secretion) rapidly
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16
Q

Penicillin resistance

A
  • Modifications/alterations in (penicillan binding proteins) PBPs → decreased drug binding and subsequent ↓ antibacterial activity
  • Prevent β-lactams from accessing and traversing pore channels and reaching PBPs in the cell membrane of gram-negative bacteria
  • Produce β-lactamase to inactivate β-lactams
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17
Q

Augmentin is the combination of

A

Amoxicillin + Clavulanic acid

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18
Q

Penicillin-related adverse drug reaction (opening of ß-ring forms what and what happens)

A
  • opening of b-lactam ring → benzylpenicilloyl (major determinant, 95%) and is responsible for the adverse reaction to penicillin.
  • hypersensitivity reactions
  • Type I - symptoms appear (~ an hour) in the skin, e.g., itch, urticaria; anaphylaxis in up to 0.04%
    of patients
  • Type IV - T-cell mediated
  • superinfection such as candidiasis occurs due to prolonged use
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19
Q

β-lactams (II) - cephalosporins generations and spectrum of action

A

1 → Gram+
2 → less Gram+ (compared to 1), and some Gram
3 → Gram+, and greater Gram
4 → Gram+, and even greater Gram
5 → Expanded Gram+, including MRSA ; common Gram

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20
Q

MRSA

A

(methicillin-resistant Staphylococcus aureus)

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21
Q

Cephalosporins Pharmacokinetics

A
  • acid stable
  • most are administered parenterally; a few can be administered orally
  • distribution - extracellular fluid ; some can cross blood-brain barrier to treat meningitis
  • excretion is mostly by renal tubular secretion
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22
Q

Cephalosporin-related adverse drug reaction

A
  • similar to penicillins
  • cross-reactivity between penicillins and cephalosporins
  • opening of b-lactam ring → cephalosporoyl, but is unrelated to adverse drug reaction
  • similarity of side chain between penicillins and cephalosporins (1st and 2nd gen.)

Would not give to someone allergic to amoxicillin

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23
Q

70S bacterial ribosome consists of two subunits

A
  • 50S subunit
  • 30S subunit
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24
Q

What is the S in 70S ribosome

A

[S: the Svedberg unit for sedimentation coefficient]

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25
Q

Bacteria protein synthesis steps

A
  1. Initiation (aa at a-site)
  2. Elongation (aa and met bind at A then move to P-site)
  3. Termination (E-site)
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26
Q

Bacteria protein synthesis Initaiton

A

The initiation of protein synthesis in bacteria involves a series of steps, including the formation of the 30S preinitiation complex, recognition of the AUG start codon, binding of the 30S subunit to the tRNA fMet at the P site, and the union of the 50S component with the 30S initiation complex to form the 70S initiation complex.

27
Q

Bacteria protein synthesis Elongation

A

Key steps in this phase include the arrival of the next tRNA at the A site, formation of the peptide bond, and the shifting of the mRNA through the ribosome by one codon after the peptide bond has been formed.

28
Q

Bacteria protein synthesis Termination

A

Steps involved in the termination phase include the arrival of a stop codon in the mRNA at the A site, recognition of the stop codons by release factors, and the subsequent termination of translation, release of the polypeptide from the tRNA and dissociation of the 70S ribosome into its 30S and 50S subunits.

29
Q

Aminoglycosides are bacteria -cidal or -static

A

bactericidal

30
Q

Tetracyclines, Amphenicols and antibacterial macrolides are bacteria -cidal or -static

A

Bacteriostatic

31
Q

What does aminogylcosides affect in protein synthesis and how

A

initiation
[30S] inhibit codon-anticodon interaction;
cause mRNA misreading

32
Q

What does tetracyclines affect in protein synthesis and how

A

tRNA binding
[30S] inhibit aminoacyl-tRNA binding to the A site

33
Q

What does amphenicols affect in protein synthesis and how

A

transpeptidation
[50S] inhibit peptide bond formation

34
Q

What does antibacterial macrolides affect in protein synthesis and how

A

Elongation and translocation
[50S] prevent transfer of tRNA with the growing peptide from A site to P site

35
Q

Aminoglycosides inhibit

A

inhibit codon-anticodon interaction, causing mRNA misreading

36
Q

Aminoglycosides: Spectrum of action

A
  • Gram- bacteria and some Gram+ bacteria
37
Q

Aminoglycosides graph

A

time- and concentration-dependent - AUC:MIC

38
Q

Pharmacokinetics of Aminoglycosides

A
  • administered intramuscularly or intravenously (not absorbed from the GI tract)
  • elimination by glomerular filtration (urine)
39
Q

Ototoxicity and nephrotoxicity of Aminoglycosides

A

ototoxicity
* hearing loss and impaired vestibular functions
nephrotoxicity
* accumulation in proximal tubular epithelial cells

Deal: inhibit accumulation by inhibit tranporter of that drug to proximal tube so no accumulation to decrease risk of nephrotoxicity

40
Q

Tetracyclines inhibit

A

inhibit aa-tRNA binding to the A site

41
Q

Tetracyclines: Spectrum of action

A
  • broad spectrum of action - Gram- and Gram+ bacteria
42
Q

Tetracyclines: Pharmacokinetics administration

A

Administered generally orally but can also be administered parenterally

43
Q

Tetracyclines and Gastrointestinal disturbance

A

Direct irritation and modification of gut flora following prolonged use

44
Q

Tetracyclines and Calcium chelation

A
  • tetracycline accumulation in teeth and growing bones
  • staining and bone deformities - avoid in children and pregnant women (category D)
45
Q

Tetracyclines cause 2 adverse

A

Gastrointestinal disturbance
Calcium chelation

46
Q

Amphenicols inhibit

A

inhibit peptide bond formation

47
Q

Amphenicols: spectrum of action

A

broad spectrum of action - Gram- and Gram+ bacteria
Static

48
Q

Amphenicols: Pharmacokinetics

A
  • chloramphenicol*
  • rapid absorption following oral administration
  • hepatically cleared (UGT2B7; 10% excreted unchanged in the urine)
49
Q

Amphenicols and Bone marrow suppression

A

idiosyncratic; pancytopenia - ↓ in all blood cell elements

50
Q

Amphenicols and Grey baby syndrome

A
  • insufficient hepatic glucuronidation and excretion in newborns
51
Q

Antibacterial macrolides prevent what

A

prevent transfer of tRNA with the growing peptide from A site to P site

52
Q

Antibacterial macrolides: spectrum of action

A

Similar spectrum of action to penicillins - useful alternatives
* concentrated within phagocytes - enhance intracellular killing of bacteria

53
Q

Antibacterial macrolides: Pharmacokinetics

A
  • oral (common) or IV administration
  • substrates for and inhibitors of CYP3A4 - drug-drug interactions
54
Q

Antibacterial macrolides cause

A

Gastrointestinal disturbance

55
Q

Mechanisms of resistance to aminoglycosides

A

drug modification

56
Q

Mechanisms of resistance to tetracyclines

A

active efflux of the drug from the cell

57
Q

Mechanisms of resistance to chloramphenicol

A

target modification (ribosomal RNA or proteins)

58
Q

Mechanisms of resistance to macrolides

A

target modification (ribosomal RNA or proteins); drug degradation (by esterases)

59
Q

Inhibit bacterial cell wall synthesis

A

Penicillin and Cephalosporins

60
Q

Inhibit protein synthesis

A

Aminoglycosides
Tetracyclines
Amphenicols
Marcolides

61
Q

Which bacterial cell wall has less peptidoglycan layers (gram +/-)

A

Gram-negative

62
Q

Which bacterial cell wall has more peptidoglycan layers than the other cell wall (gram +/-)

A

Gram-postive bacteria

63
Q

How does Augmentin work?

A

Amoxicillin works by interfering with the synthesis of bacterial cell walls, a process crucial for bacterial survival. Dependent on the intact beta-lactam ring in the amoxicillin molecule. Beta-lactamase enzymes produced by some bacteria can break this ring, rendering amoxicillin ineffective.

Clavulanic acid acts as a beta-lactamase inhibitor. This prevents the enzymes from breaking the beta-lactam ring of amoxicillin.

By inhibiting beta-lactamase enzymes, amoxicillin reaches target sites inhibit cell wall synthesis, and ultimately kill the bacteria or stop their growth.

The combination of amoxicillin and clavulanic acid (Augmentin) thus becomes effective against a wider range of bacteria, including those that produce beta-lactamase enzymes and would otherwise be resistant to amoxicillin alone.

PHAR221 (23 decks)

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