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Phar 506 > Antibiotic: Protien Synthesis inhibitors > Flashcards

Antibiotic: Protien Synthesis inhibitors Flashcards

1
Q

What is the MOA of macrolides

A

Inhibits protein synthesis when specific mRNA sites are present that would lead to certain amino acid sequences

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2
Q

What are the common macrolides

A

Clarithromycin, Azithromycin, Roxithromycin

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3
Q

T/F: The first macrolide antibiotic was erythromycin

A

True

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4
Q

What gram stain type of bacteria do macrolides work best on

A

Gram positive

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5
Q

What was the main problem with 1st generation macrolides

A

At acidic pHs they would become unstable and convert into an inactive ketal

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6
Q

What subunit do macrolides bind to, where on the this subunit does it cause problems

A

Large subunit, nascent protein tunnel

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7
Q

What part of macrolides binds to ribosome, with is the nucleotide that is bound

A

Desosamine binds to A2058

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8
Q

What structure changes of third generation macrolides make them improved

A

alkyl-aryl side chain of ketolides make additional contacts with the ribosome, increasing affinity of the drug

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9
Q

What are the three main types of antibiotic resistance

A

Ribosome modification, drug efflux, ribosome protection

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10
Q

T/F: Mutations in rRNA are rare and occur mostly in organisms with low copy numbero of rRNA genes

A

True

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11
Q

What is the most frequent mechanism of macrolide resistance

A

Dimethylation of A2058 by Erm

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12
Q

What is the protein that actively removes macrolides from their site of action

A

MrsE

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13
Q

What is the MOA of oxazolidinones

A

Binds the peptidy transferase center preventing the initiation of translation

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14
Q

What are the two common oxazolidinones

A

Linezolid and Tedizolid

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15
Q

What gram stain type of bacteria do oxazolidinones work best on

A

Gram positive

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16
Q

What subunit does oxazolidinones bind to, where on that subunit, what specifics need to be present for binding

A

Large subunit, the peptidyl transferase center, a penultimate alanine on the growing peptide

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17
Q

What is the main adverse effect that comes from using oxaolidinones, why

A

reversible myelosuppression, mitcohondria rRNA are quite similar to bacterial rRNAs and therefore are also effected

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18
Q

What are the genes that lead to oxazolidinone resistance, what can their expression lead to

A

cfr, methylation of A2503

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19
Q

T/F: Expression of erm and cfr genes could lead to resistance to all clinical antibiotics that target the large ribosomal subunit

A

True

20
Q

What is the MOA of lincosamides

A

Binds near the peptidyl transferase causing a steric hinderance that inhibits the elongation causing premature dissociation

21
Q

What is the most used lincosamide

A

Clindamycin

22
Q

What gram stain does lincosamide (clindamycin) antibacterials work on

A

Gram positive

23
Q

What are the mechanisms of resistance for lincosamides (clindamycin)

A

Erm dimethylation of A2058, Adenylation, Efflux transporters expressed

24
Q

What are the two parts of streptogramin

A

Streptogramin A (Daflopristin) and Streptogramin B (Quinuprisitn)

25
Q

Where do the two streptogramins bind

A

Streptogramin A (Dafloprstin) binds near the peptidy transferase center and Streptogramin B (Quinuprisitn) binds the nascent peptide tunnel

26
Q

T/F: When only one streptogramin binds it is bacterocidial but when both binds they become bacteriostatic

A

False: Streptogramins have synergy that allows their combination to be bactericidal

27
Q

What is the mechanism of synergy for streptogramins

A

Binding of dalfopristin remodles the rRNA structure stimulating binding of quinupristin

28
Q

What are the mechanisms of resistance for streptogramins

A

Vat acetyltransferase adds acetyl group to dalfopristin, Vgb lyase opens circle for quinupristin, Erm methyltransferase dimethylates A2058

29
Q

What is the MOA of aminoglycosides

A

Aminoglycosides take the place of two nucleotides in the decoding center that conform correct codon/anticodon interactions, there is no more checking wrong amino acids are incorporated in growing protein

30
Q

What subunit do aminoglycosided bind, where on that subunit

A

small subunit, the decoding center

31
Q

What gives aminoglycosides their selectivity

A

The nucleotide 1408 of the small subunit rRNA is A while in eukaryotes it is G

32
Q

T/F: Aminoglycosides are nephrotoxic and ototoxic

A

True

33
Q

What are enzyme and enzyme functions that lead to resistance to amnioglycosides

A

ArmA/RmtA methtransferase methylates G1405 near the aminoglycoside site, NpmA rRNA methyltransferase modifies A1408

34
Q

What are changes to the drug structure of aminoglycosides that leads to resistance

A

the drug becomes N-acetylated, O-phosphorylated or O-adenylated causing steric hinderance that prevents binding to the target

35
Q

What makes streptomycin different from other aminoglycosides

A

It has the same the MOA but a different binding site

36
Q

Why are older generations of tetracyclines more reactive

A

Ring A can undergo renolization and protonization that could potentially cause it to lose half of its activity

37
Q

What is the MOA of Tetracyclines

A

Tetracycline binds where tRNA would bind not allowing the correct matchups to happen between codons and anticodons

38
Q

What subunit of the ribosome does tertracycline bind to

A

Small subunit

39
Q

What are the mechanisms of resistance against tetracylcines

A

Tet(M) or Tet(O) evict the drug from the ribosome (Ribosome protection), Tet(A) or Tet(B) remove the drug from the ribosome (efflux pumps)

40
Q

What does RNA polymerase do

A

convert DNA into messenger RNA (transcription)

41
Q

T/F: Rifampicin is an inhibitor of transcription and binds the alpha subunit

A

False: Rifampicin binds in the exit of the RNA tunnel in the Beta subunit of RNA polymerase and inhibits formation of the second or third phosphodiester bonds

42
Q

T/F: Sulfonamides are bacteriocidial and have no structural analogs

A

False: Sulfonamides are bacteriostatic antibiotics and are a structural analog to PABA

43
Q

How do sulfonamides cause less nucleotides and amino acids available to the cell

A

Sulfonamides competitively competes with PABA for Dihydropteroate synthaase causing less Folic acid and tetrahydrofolate which is a precursor to nucleotides and amino acids

44
Q

How do adding electron withdrawing groups aid in solubility and potency of the drug

A

reducing the pKA of amino group closer to what PABAs also allowing solubility at neutral pH leading to know crystalization in the kidneys

45
Q

How does trimethoprim act synergistically with sulfonamides, what enzyme

A

Trimethoprim acts upon another enzyme in the same pathway that is inhibited by sulfonamides, dihydrofolate reductase

Phar 506 (37 decks)

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