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Pharmacy Stage 2 > Antibiotic Chem 1 and 2 > Flashcards

Antibiotic Chem 1 and 2 Flashcards

1
Q

6 ways antibiotics cure bacteria infections?

A

1) inhibit bacterial cell wall synthesis
2) inhibit protein synthesis
3) inhibit nucleic acid transcription and replication
4) Injury to plasma membrane
5) Inhibit synthesis of essential metabolites
6) Miscellaneous (collection of various types of methods)

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2
Q

Difference between gram positive and gram negative bacteria cell wall?

A

1) Gram positive has 1 phospholipid bilayer, gram negative has 2 bilayers
2) Gram positive has lipoteichoic acid, gram negative doesn’t.
3) Gram positive has teichoic acid, gram negative doesn’t
4) peptidoglycan and beta lactamase on outside of phospholipid for gram positive. For gram negative, they’re inbetween the 2 phospholipid bilayers in the periplasmic space.

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3
Q

Role of penicillin in inhibiting bacterial cell wall synthesis?

A

Inhibits the transpeptidase enzyme by binding irreversibly to the serine residue on the transpeptidase enzyme so the peptidoglycan molecules can’t bind at their active site. This inhibits the cell wall being synthesised as the peptidoglycan molecules can’t be cross-linked together to form the cell wall.

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4
Q

Adverse drug reactions from using beta-lactams?

A

1) Anaphylaxis
2) Urticaria (hives)
3) Steven-Johnson Syndrome
4) Acute exanthematic pustulosis
5) Drug hypersensitivity syndrome

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5
Q

Two types of drug hypersensitivity syndromes?

A

1) IgE mediated response (occurs immediately)

2) T cell mediated response (Delayed reaction)

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6
Q

What happens during penicillin hypersensitivity?

A

The penicillin beta-lactam ring is cleaved by low pH conditions, by the presence of metal ions or by nucleophiles.

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7
Q

How does MRSA work?

A

Produces a Penicillin Binding Protein 2 (PBP-2) which doesn’t bind to methicillin as effectively so can’t be inhibited/destroyed by methicillin antibiotic.

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8
Q

Which carbon side chain in penicillin undergoes acid hydrolysis?

A

The C-6 side chain.

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9
Q

What is used to treat MRSA?

A

Vancomycin

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10
Q

How does vancomycin inhibit cell wall synthesis?

A

contains 4 H-Bond Donors and 1 H-Bond Acceptor group that form 5 H-bonds to terminal D-Ala-D-Ala. This inhibits a number of processes by forming a protective layer. The D-Ala-D-Ala is held in the deep cleft within the vancomycin.

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11
Q

What type of bacteria do glycopeptides inhibit their cell wall synthesis?

A

They inhibit gram positive bacterial cell wall synthesis by teichoplanin and are less toxic than vancomycin

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12
Q

Adverse drug reactions of vancomycin?

A
  • Anaphylaxis
  • hypotension,
  • Dyspnea
  • urticaria,
  • red man syndrome,
  • nephrotoxicity
  • auditory nerve damage
  • ototoxicity!
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13
Q

What is vancomycin resistance?

A

When bacteria develops resistance to vancomycin antibiotic, the bacterial cell wall precursor is modified so the D-Ala is replaced by D-lactic acid, hence removing the vancomycin H-bonds. This is the case for VRSA (vancomycin resistance staphylococcus aureus) and VRE (vancomycin resistant enterococcus )

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14
Q

What is rRNA?

A

Ribosomal RNA is a structural component of ribosomes

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15
Q

What is tRNA

A

Transfer RNA are carriers of amino acids for protein synthesis

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16
Q

What is mRNA

A

Messenger RNA is a sequence of bases that determines the amino acid sequence in protein synthesis.

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17
Q

How does streptomycin inhibit protein synthesis?

A

Changes shape of 30S ribosome hence causing the mRNA code sequence to be read incorrectly.

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18
Q

How do tetracyclines inhibit protein synthesis?

A

Interferes with the attachment of tRNA to mRNA-ribosome complex by binding to 30S ribosome. This stops further amino acid attachments and protein release.

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19
Q

How do aminoglycosides inhibit protein synthesis?

A

1) they bind to the 16 ribosomal DNA portion of the 30S ribosome. This impairs proof reading of ribosome.
2) Due to the binding on the ribosomal DNA, the peptidyl A site conformation is changed.
3) This results in mistranslation of the mRNA template and selection of incorrect amino acids.

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20
Q

How does aminoglycoside resistance work?

A

The bacteria has transfer factor mediated enzymes which acetylate, phosphorylate and/or adenylisate the aminoglycosides. This changes their chemical structure hence making them unable to function (unable to bind to 16S DNA ribosome).

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21
Q

Drug interaction between aminoglycosides and beta-lactams?

A

They react with each other and the beta-lactams can acetylate the aminoglycosides hence making them inactive.

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22
Q

What does the other binding site on tetracyclines do?

A

binds to sugar phosphate of 16S rRNA using Mg2+

23
Q

What does tetracycline interact with?

A

1) Ion rich antacids
2) Dairy products rich in Ca2+
3) Can form a complex with Ca2+ from teeth and bone
4) Imcompatible in acidic and basic conditions.

24
Q

What is the diastereiomer of tetracycline?

A

4-Epitetracycline (look at slide 11 of antibiotic chem 2)

25
Q

Problem with tetracyclines with C-6 OH groups?

A

They can dehydrate to form 4-Epianhydrotetracycline which is nephrotoxic and causes less re-absorption of materials. Without the OH group of the 6th carbon, they’d be free from this toxicity as they can’t dehydrate.

26
Q

Are macrolides basteriostatic or bactericidal antibiotics?

A

Bacteriostatic.

27
Q

What do macrolides do?

A

Inhibit ribosomal protein biosynthesis by binding to the 23S rRNA in the
polypetide exit tunnel, adjacent to the peptidyl tRNA centre in
the 50S ribosomal subunit. So it inhibits translocation (hence preventing the polypeptide chain growing).

28
Q

What does CYP 3A4 do?

A

It metabolises macrolides into nitosoalkanes. It is responsible for 50% biotransformation of all therapeutic agents.

29
Q

Is Chloramphenicol a basteriostatic or bactericidal antibiotic?

A

Bacteriostatic

30
Q

How does chloramphenicol work to inhibit protein synthesis?

A

Inhibits protein synthesis by binding to 50S ribosome subunit at the peptidyl transferase centre A site, preventing binding of next charged tRNA

31
Q

What does the catalytic site of chloramphenicol bind to?

A

Mg2+ and can also form H-bonds and other interactions.

32
Q

Why is chloramphenicol considered toxic?

A

because of the nitro group.

33
Q

What does chloramphenicol do to CYP 2C19 and 3A4?

A

It inhibits them hence slowing down metabolism (of drugs especially).

34
Q

What does Lincosamides do?

A

Binds to the 50S rRNA of the large bacterial ribosome subunit and prolongs the effects of neuromuscular-blocking drugs
Its similarity to the mechanism of action of Macrolides and Chloramphenicol means they should not be given simultaneously, as this causes antagonism and possible cross-resistance

35
Q

Are oxazolidinones basteriostatic or bactericidal antibiotic?

A

Can be both against gram positive bacteria.

36
Q

What do Oxazolidinones do?

A

1) Inhibits protein synthesis by binding to 50S subparticle preventing formation of the functional initiation complex e.g N-formylmethionine-tRNA, 30S subunit, mRNA and initiation factors
2) Distorts the binding site for initiator tRNA which overlaps both 30S and 50S
3) Competes with Chloramphenicol in binding with the 50S unit but does not have the same mode of action.

37
Q

How can we reduce resistance issues related with the use of oxazolidinones?

A

Use the antibiotic at an earlier stage of bacterial infection.

38
Q

What does DNA Gyrase do?

A

alters the conformation of DNA by catalysing double strand cuts, passing uncut portion through the gap resealing the molecule

39
Q

What does DNA topoisomerase IV do?

A

unties enchained daughter molecule.

40
Q

What do fluoroquinolones do?

A

Inhibit replication and transciption of bacterial DNA by stabilizing the
complex formed between DNA and topioisomerases.

41
Q

Are fluoroquinolones bactericidal or bacteriostatic antibiotics?

A

bactericidal

42
Q

What are Topoisomerase IV and DNA Gyrase more important to, Gram (-) or Gram (+)

A

Topoisomerase IV = Gram (+)

DNA Gyrase = Gram (-)

43
Q

Drug interactions of Fluoroquinolones?

A

1) interact with metal ions of antacids
2) inhibit CYP1A2 causing increased serum levels
3) Some quinolones reduce gut floral growth resulting in the reduction of digoxin metabolism.

44
Q

What type of bacteria does polymixinB act on to cause injury to their plasma membrane?

A

Gram negative

45
Q

How does polymixinB work?

A

Binds to phosphate groups in bacterial membranes disrupting integrity

46
Q

What types of toxicity does polymixinB cause?

A

neuro and nephro toxicity.

47
Q

What is used to inhibit the synthesis of essential metabolites when treating bacterial infections?

A

Sulfonamides and Trimethoprim

48
Q

Are Sulfonamides and Trimethoprim bacteriostatic or bactericidal?

A

bacteriostatic

49
Q

What type of inhibitors are Sulfonamides and Trimethoprim?

A

Competitive inhibitors of dihydropteroate synthetase.

50
Q

What do Sulfonamides and Trimethoprim inhibit the biosynthesis of?

A

tetrahydrofolate in bacterial cells

51
Q

Problems with drugs having high pKa values?

A

Prone to crystalluria which results in kidney damage

52
Q

Three ways to avoid crystalluria?

A

1) attach heterocyclic rings to sulfonamide to reduce pKa values making them easier to ionise hence more water soluble.
2) using more than one type of sulfonamide
3) amount of each sulfonamide given should not the reach threshold amount leading to crystal formation.

53
Q

what 4 classes are Sulfonamides and Trimethoprim grouped into?

A

1) rapidly absorbed/excreted
2) poorly absorbed
3) topical - burns
4) long acting

Pharmacy Stage 2 (85 decks)

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