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D&D Infectious Disease Midterm > Pharm - Protein Synth Inhibitors: Tetracyclines and glycylcyclines > Flashcards

Pharm - Protein Synth Inhibitors: Tetracyclines and glycylcyclines Flashcards

1
Q

tetracyclines and glycylcyclines are bacteriostatic or cidal?

A

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2
Q

macrolides are bacteriostatic or cidal?

A

static

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3
Q

erythromycin is an examples of a……..

A

macrolide

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4
Q

streptogramins are bacteriostatic or cidal?

A

cidal (in combo)

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5
Q

cloramphenicol is bacteriostatic or cidal

A

static

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6
Q

lincosamides are bacteriostatic or cidal

give an ex

A

clindamycin

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7
Q

aminoglycosides are bacteriostatic or cidal

A

cidal

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8
Q

oxazolidinones are bacteriostatic or cidal

A

static

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9
Q

most of a bacterial ribosome consists of what?

A

RNA

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10
Q

aminoglycosides act on what bacterial ribosome

A

30s

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11
Q

tetracyclines and glycylcyclines act on what bacterial ribosome

A

30s

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12
Q

____- and _____ are the only protein synthesis inhibitors that act on the 30s ribosome. all the others act on 50s

A

tetracyclines and glycylcyclines and aminoglycosides

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13
Q

the 50s subunit is the ___ ribsosome

A

the larger ribosomal subunit

30s is the smol one

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14
Q

name 3 glycylcylines

A

tigecycline
eravacycline
omadacycline

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15
Q

why were the glycylcyclines made

A

are long acting (better pharmacokinetic profile) and have a better resistance profile than tetracyclines

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16
Q

how do the glycylcyclines have a better resistance profile than the tetracyclines

A

their structure doesn’t allow for proper binding to the efflux pump

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17
Q

tetracyclines are _____ spectrum ____ antibiotics that inhibit what?

A

broad spectrum bacteriostatic that inhibit protein synthesis

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18
Q

briefly explain the MOA of tetracyclines

A

they reversibly bind to the 30s subunit of the bacterial ribosome

this blocks the binding ot the aminoacyl-tRNA to the acceptor (A) site on the mRNA-ribosome complex

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19
Q

what is the aminoacyl-tRNA

A

the tRNA that brings the amino acid

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20
Q

how do tetracyclines enter the bacteria

A

by passive diffusion and in part by active transport (energy dependent)

21
Q

true or false

tetracyclines are only active against gram negative bacteria

A

FALSE - broad spectrum
gram (+) and (-)

22
Q

what are tetracyclines NOT very active against

A

pseudomonas, neisseria, enterobacter

23
Q

3 methods of tetracycline resistance

A
  1. decreased influx of the AB OR getting an efflux pathway
  2. bacteria produce a protein that protects the ribosome - displaces the tetracycline from its 30s target
  3. enzymatically inactivated
24
Q

name 3 different efllux pumps that bacteria can produce against tetracyclines

include what bacteria produce them and what they provide resistance to

A

Tet (AE) efflux pump - produced by gram negative species. provides resistance against tet,doxy, and mino - BUT NOT TIGECYCLINE

Tet (K) efflux pump - produced by staphylococci. provides resistance to tetracycline but NOT doxy, mino, or tigecycline

proteus and pseudomonas produce their own specific efflux pump that gives resistance to ALLL - tetracyclines and tigecycline

25
Q

as mentioned, a mechanism of resistance to tetracyclines is the production of a ribosomal protection protein

name 2 of these proteins and what they are/aren’t resistant to

A

tet(M) and tet(O)

resistant to doxy, tet, and mino, BUT STILL SUSCEPTIBLE TO TIGECYCLINE

therefore, tigecycline overcomes 2 resistance mechanisms

26
Q

what other antibiotic class has a similar resistance mechanism of protection proteins

A

fluoroquinolones — QNR proteins

27
Q

how can the absorption of tetracyclines be impaired

A

when given with divalent and trivalent cations (like quinolones)

do not give dairy products or antacids

28
Q

the oral absorption of most tetracyclines is……

A

incomplete

29
Q

how is tigecycline administered

A

NOT ABSORBED WELL – only parenteral

30
Q

concern with tetracyclines

A

-cross placenta and excreted in breast milk

-cause damage to growing bones and teeth!!!

31
Q

explain the DDIs of tetracyclines

A

there are a lot. many drugs like carbamezepime, phenytoim, barbiturates, and alcohol decrease the half life by 50% — so need to increase dose

32
Q

______ is a substrate of CYP3A4, so there are many potential drug-drug interactions

A

eravacycline

33
Q

true or false

tetracyclines have good activity against anaerobes

A

true

(how to remember - they’re used in acne)

34
Q

name 5 things in which tetracyclines are drug of choice

A

rickettsia
borrelia
mycoplasma pneumonia
chlamydia
some spirochetes

35
Q

true or false

tetracyclines can be used for CAP

A

true

36
Q

can tetracyclines be used for MRSA

A

mild-moderate MRSA

37
Q

true or false

tetracyclines can’t be used in lyme disease

A

false - they can

38
Q

true or false

tigecycline is broad spectrum bacteriostatic

A

true

high potency against range of both gram (+) and (-)

39
Q

TRUE OR FALSE

tigecycline is not active against MRSA

A

false - it is

40
Q

how is tigecycline administered and how eliminated

A

IV only

eliminated through bile - no dose adjustment for renal insufficiency!

41
Q

eravacycline is a _________ tetracycline for _______

A

fluorinated

complicated intrabdominal infections

42
Q

main adverse affects of all tetracyclines

A

GI -NVD(because broad)
photosensitivity
hepatoxicity
nephrotoxicity
discolor teeth and affect bone growth

FANCONI SYNDROME (only for expired) — sugars and electrolytes not reabsorbed back into the body

43
Q

can tetracyclines be used in pregnancy

A

NO - teratogenic

44
Q

true or false

production of Tet(M) protein is a resistance mechanism against tigecycline

A

FALSE — tigecycline is resistant to this mechanism

45
Q

chemically, what is tigecycline

A

a glycylcycline

46
Q

what does the extended structure of tigecycline allow for

A

resistance doesn’t happen as much as tetracyclines

47
Q

true or false

tigecycline is active against MRSA

A

true

48
Q
A

D&D Infectious Disease Midterm (26 decks)

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