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anibiotics > Protein Synthesis Inhibitors > Flashcards

Protein Synthesis Inhibitors Flashcards

1
Q

From which be bacterial species do we obtain aminoglycosides?

A

Streptomyses 1943

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2
Q

What biochemically active structure to the aminoglycosides drugs contain ?

And what does it consist of?

A

Linked ring system , amigos sugars and polyalcohols

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3
Q

How should aminoglycosides be administered to the body?

What bacteria does this drug target ?

A

Poor oral absorption (give IV),

potent broad spectrum

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4
Q

Examples of aminoglycosides?

A

(Mycin) strepto, kana, tobra, neo, genta and amikacin

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5
Q

What organism do aminoglycosides have good coverage?

A

Gram negative bacilli and staphylococci

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6
Q

What organisms do aminoglycosides have poor coverage?

A

Anaerobes and streptococci

NB. However active with penicillin (synergists)

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7
Q

How well are aminoglycosides absorbed into tissues etc.?

How does this reflect on its administration/clinical use?

A

Poor mammalian cell penetration!
, hence … Not got for intracellular organism

-instead septicaemia and endocarditis

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8
Q

Dangers/ Sid effect of aminoglycosides ?

A

Ototoxic & nephrotoxic

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9
Q

Aminoglycosides- mode of action

1) this molecule binds to ribosome and does what?

A

Non functioning initiating complexes, Inhibits translocation step of protein synthesis causing misreads of mRNA transcript - causing defective proteins

(Does not fully explain potent bacteriocidal properties)

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10
Q

Aminoglycosides- cell penetration and entry

A
  • enter cell via active transport, self regulated uptake via dysfunction proteins disorganising membrane further.
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11
Q

Aminoglycosides - resistance mechanism (x2)

A

Alteration of ribosome structure (target change)

Aminoglycosidic modifying enzyme (enzymatic)

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12
Q

Remember drugs via ; “CLEan TAG” …. explain?

A

Oral, Chloramphenicol and Clindomycin
Oral, Lincosamides
Oral, Erythromycin

IV, Tetracycline and tigicylcine
IV, AminoGlycosides

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13
Q

What species are tetracyclines derived from?

A

Streptomyces aurofaciens 1948

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14
Q

What organisms do tetracycline have good coverage of?

A

V. Broad spectrum drugs
Gram -ive and +ive rickettsia,chylamidia, mycoplasma and spirochetes
(NB similar activity, but Pharmokinetically different)

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15
Q

Which drugs come under “natural tetracyclines “

A

Chlortetracycline
Tetracycline
Oxytetracycline

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16
Q

Which drugs come under semi-synthetic ?

A

Doxycycline

Minocycline

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17
Q

What are the clinical implications of semi-synthetic tetracyclines

A

Once/twice daily (long H.F)
lower renal toxicity
Better than other when taken orally!

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18
Q

Tetracyclines - penetration and action

So when susceptible bacteria are exposed to gees drugs what happens?

A

Bacteria concentrate tetracyclines via active transport (bacteria static)
interact with 30 subunit (TAG)
Interfere with tRNA binding to A site on ribosome

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19
Q

How does resistance to tetracyclines occur normally?

A

Via production of new proteins that prevent accumulation in cohort with effluent mechanism, purveying resistance to all of here drugs

NB, ECEPT tigecycline avoids this due extreme affinity for ribosome

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20
Q

From which organism is chloramphenicol derived

A

Streptomyces 1940’s

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21
Q

Chloramphenicol, what are the pro’s of this drug.?

A

Broad spectrum agent

Simple organisation - easy to synthesise

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22
Q

For which organisms does this drug have good coverage ?

How? Briefly …

A

Broad spectrum
G-Ive and G+ive, rickettsia chylamidia

Target 70s ribosome, thus largely bactiostatic but is bacteriocidal to some.

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23
Q

Chloramphenicol - clinical implications

A

Defuses well into CSF.

Thus, used for meningitis and typhoid (intracellular)

24
Q

How does resistance occur to chloramphenicol ?

A

Normally enzymatic, acylating two OH groups

However uncommon. Problem in Dev. World

25
Q

what are the side effects of chloramphenicol

A

aplastic anaemia.
used for life threatening infections only.
or
when sae therapies failed/infection is resistant

26
Q

neonatal side effects on chloramphenicol ?

A

liver incapable of detoxification enough drug, sufficient to kill bacteria, leads to – hypotention, c.v collapse, grey baby syndrome(fatal)

27
Q

chloramphenicol applications and implications on bone marrow side effects.

A

Dose related BM suppression (4g/m a day- reversible).
Total BM depression & aplastic anaemia rare! (mortality. >50%).
Now used topically, rarely used systemically
Cheap (dev. world & typhoid fever/ meningitis

28
Q

From what organism is “Fusic Acid” derived?

A

Fusidium 1960’s

29
Q

Molecularly how does Fusic acid inhibit protein synthesis?

A

Prevents translocation step in protein synthesis via inhibition of “elongation factor G” recycling.

30
Q

what organism does Fusic acid have good coverage

A

in vitro active against gram positive & negative, however G-ive prevent acess through membrane.
clinically used for staph. inf. only!

31
Q

any good clinical feature of Fusic acid as atibiotic?

A

good bone and tissue penetration - osteomyelitis.

32
Q

Resistance to Fusic acid? if so how (we think)?

A

resistance variants in any population, single point mutation renders resistance, proliferative with therapy ADD another antibiotic!

33
Q

side effects of Fusic acid ?

oral?
IV
topical?

A

no problem,
reversible jaundice
non, but resistance risk!

34
Q

From which organism is a macrolide derived?

A

streptomyces erythrens

35
Q

Macrolides, how do they work?

A

cause dissociation of growing peptide chain from ribosome during translocation

36
Q

antibiotic coverage of macrolides?

A

usually used for staphylococcal and streptococcal inf., but als legionella chlamydia and mycoplasma.
(good cellular penetration for intracellular)

37
Q

side effects and resistance issues, of Fusic acid?.

A

nausea and abdominal cramps.

resistance = modification of 50s rRNA or enzyme inactivation.

38
Q

Macrolides how are they given and absorbed?

A

erythromycin, enteric coat ->SoA small intestine.
Azithromycin, semi synthetic , long HL in blood & tissues.
Clarithromycin, better absorbed, fewer side effects.

39
Q

from which organism does mupirocin derive?

A

pseudomonas flourescens

40
Q

How does Mupirocin function as antibiotic?

A

blocks incorporation of amino acid into poplypeptides.

41
Q

What organisms does mupirocin have good coverage?

A

staphylococi and streptococci sp.

42
Q

clinical applications of mupirocin?

A

inactivated when used topically
sometimes used for nasal carriage of staph. MRSA!
in particular..

43
Q

streptogramins originate from which organism

A

streptomyces sp.

44
Q

streptogramins, in organisation and funtion. what are they?

A

cyclic peptides administered in combination with/from two groups A + B, alone feeble, together potent.

45
Q

within combination streptogramin antibiotic regimes ,

quinopristin?

dalfopristin?

A

premature release of peptide chain
&
prevents peptide elongation

46
Q

streptogramins, organism coverage?

A

use for Vanc. resistant enterococci (VRE) E. faceium only!, no activity against other similar sp.

47
Q

Lincosamides derive from which organism?

A

Streptomyces lincolnensis

48
Q

lincosamides, how does is work?,

A

interfere with peptide elongation, exact mechanism unsure ??

49
Q

Lincosamides, good coverage for which organisms?

A

Treat Gram positive cocci and anaerobes
• No action against the Gram negative bacilli
• Associated with Clostridium difficile infections

(clindamycin)

50
Q

oxazolidinones 1978, is a narrow spectrum dug for mainly which organisms?

A

staphylococci, pneumonococci & enterococci

51
Q

Oxazolidinones, how are they taken and how do they work?

A

orally well absorbed.

target 23s ribosomal RNA in he 50s subunit - this prevents formation of a functional 70 complex.

52
Q

oxazolidinones, resistance occurrence?

linezolid

A

resistance is slow to occur, (mutation in 23s RNA).
no cross resistance with other drugs.
reserved for resistant organisms - VRE, MRSA & TB

53
Q

oxazolidinones - side effects?

A

limited use - effect on bone marrow cells, limits use to a fortnight.

54
Q

oxazolidinones -most recently a cross resistance has occured with chloramphenicol mutation CFr… how is this resisting these drugs?

A

resistance occurs within RNA methyl transferase - enzyme modifying target.
Also gives resistance to streptogrammins, lincosamiddes, chloramphenicol and pleuromutlins (topical antibiotic MRSA).
this transferable plasmid adds CH3 to RNA (in particular 23s RNA)

55
Q

Orthomycins, what are they how do they work?

A

Oligosaccharide based.

Blocks tRNA attachment to 30s ribosomal subunit.

56
Q

orthomycins - narrow spectrum for which organisms?

A

staph, strep, entero an clostridium
possible interest for resistant organisms
however has been used as growth promotorin animals (avilamycin), so a similar resistance may already be here!

57
Q

What key targets do protein synthesis inhibitors work on to produce such bacteriocidal/static effects ?

A

The drugs work via exploiting 70s (50 &30) ribosomal subunits.

Specifically structural differences and affinity towards prokaryote ribosomes

(NB. Tetracyclines also effect eukaryotic - Protozoa)

anibiotics (4 decks)

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