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Medical Pharmacology > Protein Synthesis Inhibitors (Antimicrobials) - 30S Inhibitors > Flashcards

Protein Synthesis Inhibitors (Antimicrobials) - 30S Inhibitors Flashcards

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USMLE® Step 1 flashcards
1
Q

what drugs are protein synthesis inhibitors?

A 
gentamicin
tobramycin
tetracycline
doxycycline
tigecycline
azithromycin
erythromycin
fidaxomicin
chloramphenicol 
clindamycin
linezolid 
mupirocin
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2
Q

which agents bind to 30S ribosomal subunit

A

aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin –GNATS)

tetracyclines (doxycycline, tetracycline, minocycline)

glycylcycline (tigecycline)

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3
Q

which agents bind to 50S ribosomal subunit

A

macrolides (azithromycin, erythromycin, clarithromycin)

Chloramphenicol
Clindamycin
Erythromycin
Linezolid (oxazolidinone)

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4
Q

gentamicin route

A

topical, IV, IM

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5
Q

tobramycin route

A

topical, IV, IM, nebulized

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6
Q

general MOA of aminoglycosides

A

active transport across cell membrane into the cytoplasm by oxygen dependent process (so covers aerobes)

AND passive diffusion via porin channels across outer membrane (gram-)

(this is important)

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7
Q

what do aminoglycosides do

A

bactericidal (bc irreversible binding to 30S and formation of aberrant proteins

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8
Q

what does irreversible binding of 30S by aminoglycosides do

A
  1. interferes with initiation complex of peptide formation - blocks
  2. prevents proofreading of transcript (incorporation of incorrect AA) – miscoding
  3. blocks movement of ribosomes after single initiation complex resulting in mRNA chain with just one ribosome – block translocation
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9
Q

spectrum of aminoglycosides

A

aerobic gram - including pseudomonas

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10
Q

what would happen if you gave an aminoglycoside with a cell wall agent for gram+

A

alone aminoglycoside wouldn’t work, but once cell wall agent destroys cell wall (give first) then aminoglycoside can penetrate
(aka synergy with cell wall agents on gram+ organisms)

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11
Q

how is resistance conferred against aminoglycosides

A
  1. production of transferase enzyme that inactivates aminoglycosides
  2. imapired entry (decreased uptake and altered porins)
  3. mutation of receptor on 30S ribosomal subunit (prevents aminoglycosides from binding)
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12
Q

absorption of aminoglycosides

A

poorly absorbed, almost entire dose excreted in feces

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13
Q

when does peak concentration occur in IM

A

within 30-90min

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14
Q

peak concentration in IV

A

30-60min

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15
Q

tissue concentration of drug?

A

low because poorly absorbed

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16
Q

CNS concentration of drug

A

inadequate even with inflamed meninges

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17
Q

where do aminoglycosides accumulate?

A

renal cortex, endolymph and perilymph of the inner ear

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18
Q

side effects of aminoglycosides

A

nephrotoxicity and ototoxicity (ringing of ears)

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19
Q

aminoglycosides and placenta

A

can cross placental barrier and accumulate in fetal plasma and amniotic fluid

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20
Q

toxicity of aminoglycosides

A
  1. since high concentrations in renal cortex, endolymph and perilymph of inner ear, then nephrotoxic and ototoxic
  2. neuromuscular blockade
  3. contact dermatitis
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21
Q

what is oto and nephrotoxicity associated with

A

prolonged high trough levels (not peak levels)

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22
Q

what is neuromuscular blockade associated with

A

direct intraperitoneal or intrapleural application of a large dose

(cannot get into the CNS but can directly administer)

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23
Q

how are aminoglycosides cleared

A

renally – excretion is directly proportional to creatinine clearance

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24
Q

why must aminoglycosides be monitored in kidney damage?

A

excretion is directly proportional to creatinine clearance so if kidney not working, less excretion

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25
Q

describe aminoglycosides dosing

A 
concentration dependent (looking for a high peak)
with a post antibiotic effect (continues after drug wears off)
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26
Q

when would once daily dosing be avoided?

A
  1. renal impairment because accumlates
  2. pregnancy (crosses placenta)
  3. neonates (accumulates in fetal plasma and amniotic fluid)
  4. bacterial endocarditis
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27
Q

how to monitor aminoglycosides that are dosed once daily

A

check trough to makes sure the drug is washing out – don’t need to check peak

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28
Q

what is the goal trough for aminoglycosides dosed once daily

A

less than 1mcg/mL between 18-24hours after dosing

29
Q

how to monitor aminoglycosides for traditional dosing

A

check peak and trough levels because want it in certain range

30
Q

goal peak for traditional dosed aminoglycosides

A

5-10mcg/mL

31
Q

goal trough for traditional dosed aminoglycosides

A

less than 2mcg/mL (less than 1 optimal)

32
Q

how many half lives to steady state

A

4-5

33
Q

what is a peak?

A

drug level 1 hour ish after administration

34
Q

what is a trough

A

drug level right before next dose is due

35
Q

why do we not have to be at steady state for aminoglycosides?

A

post antibiotic effect allows washout period with decreased side effects while still allowing action

36
Q

when would washing out not be beneficial?

A

when kidney damaged bc can’t wash out anyway

37
Q

when to draw levels for aminoglycosides?

A

wait until reach stead state–4-5th dose

38
Q

what are the tetracyclines?

A

tetracycline, doxycycline, minocycline

39
Q

new tetracyclines

A
  1. eravacycline
  2. omadacycline
  3. serecycline
40
Q

what do tetracyclines do

A

bacteriostatic

41
Q

why are aminoglycosides bactericidal

A

irreversible binding to 30S subunit and formation of aberrant proteins that interfere with initiation complex of peptide formation

42
Q

why are tetracyclines bacteriostatic

A

reversibly bind to 30S subunit

43
Q

MOA of tetracyclines

A
  1. passive diffusion and energy dependent protein mechanism
  2. reversibly bind to 30S subunit, blocking access of tRNA to mRNA at acceptor site
44
Q

spectrum of tetracyclines

A 
broad spectrum 
1. many gram+ including community acquired MRSA 
gram -
2. toxin secreters (cholera)
3. rickettsiae
4. spirochetes
5. mycoplasma (intracellulars)
6. chlamydia (intracellulars)
45
Q

what diseases do tetracycline work against

A

community acquired MRSA

  1. COPD exacerbations
  2. rocky mountain spotted fever
  3. borrelia
  4. mycoplasma
  5. chlamydia
  6. minocycline for acne
  7. brucellosis
  8. erlichiosis
  9. granuloma inguinale
  10. h pylori
  11. vibrio
46
Q

how can resistance against tetracyclines occur

A
  1. impaired influx or increased efflux by active transport
  2. ribosome protection due to productions of proteins that interfere with tetracycline binding to the ribosome
  3. enzymatic inactivation
47
Q

which drugs can work against tetracycline resistant strains?

A

doxycycline or minocycline because they are poor substrates for efflux pump that mediates resistance

48
Q

kinetics of tetracyclines

A

incompletely absorbed by mouth

49
Q

which abx are not to be taken with diary, Mg, aluminum antacids or iron

A

tetracyclines and fluroquinolones

50
Q

what can not be taken with tetracyclines and why

A

dairy, magnesium, aluminum antacids and iron because they form nonabsorbable chelates

51
Q

where are tetracyclines metabolized

A

liver

52
Q

why can’t children or pregnant women get tetracyclines

A

concentrates in tissues with high calcium content so chelates with teeth and cause grey brittle teeth. also crosses the placenta and accumulates in fetal tissue.

53
Q

tetracyclines in pregnancy

A

crosses placenta, bad in pregnancy

54
Q

adverse effects of tetracycline

A
  1. photosensitivity
  2. chelation (calcium deposited in newly formed bones or teeth)
  3. gastric discomfort (do not take with dairy and antacids, but take with food)
  4. ototoxicity
  5. pseudotumor cerebri
  6. hepatotoxicity
  7. nephrotoxicity
55
Q

tetracyclines in children

A

do not give in children under 8yo

chelate to calcium deposited in newly formed bone or teeth

56
Q

what occurs if you take out of date tetracycline?

A

could cause nephrotoxicity and renal tubular acidosis

57
Q

which abx cause photosensitivity

A

tetracyclines, sulfonamides, fluroquinolones

58
Q

what ADE can demeclocycline cause

A

nephrogenic diabetes insipidus by blocking tubule cell response to ADH

59
Q

what can demeclocycline treat?

A

syndrome of inappropriate ADH (SIADH)

60
Q

MOA of tigecycline

A

reversibly binds to 30S ribosome interfering with tRNA binding

61
Q

what is tigecycline

A

bacteriostatic

62
Q

stectrum of tigecycline

A

broad spectrum
MRSA
acinetobacter
gram negatives EXCEPT PSEUDOMONAS, PROTEUS, PROVIDENCIA

63
Q

what does tigecyclines NOT effective agaist

A
  1. pseudomonas
  2. proteus
  3. providencia
64
Q

what conditions is tigecyclines used for

A

complicated skin/soft tissue, intraabdominal infections where MRSA is likely, community acquired pneumonia

65
Q

ADE of tigecycline

A 
chelation (not with oral cations bc is IV only) 
n/v/d
hepatotoxicity
phototoxicity
pseudotumor cerebri
66
Q

distribution of tigecycline

A

rapid distribution to tissues (so don’t use for bacteremia)

67
Q

why can’t tigecycline be used for bacteremia

A

rapid distribution goes to tissues fast, so don’t stay in bloodstream. would be ineffective.

68
Q

why can’t tigecycline be given in pregnancy or kids

A

risk of chelation with calcium high tissues (fetus)

Medical Pharmacology (13 decks)

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