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PC2 > Aminoglycosides > Flashcards

Aminoglycosides Flashcards

1
Q

Aminoglycosides that end in mycin

A

derived from streptomyces

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2
Q

Aminoglycosides that end in icin

A

derived from another organism or synthetic derivative

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3
Q

Aminoglycosides structure

A

2 hexanose structures on either end and a 2-deoxystreptamine

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4
Q

Aminoglycosides modifications helped to improve

A

activity, prevent resistance, and decrease adverse events

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5
Q

Aminoglycosides structure is unique because it is a

A

nucleophile

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6
Q

Aminoglycosides like to donate

A

electrons

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7
Q

Aminoglycosides is easily modified to

A

an inactive substance

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8
Q

Aminoglycosides MOA membrane penetration:

A
  1. aminoglycoside self promoted uptake process involves drug-induced disruption of Mg2+ bridges between adjacent lipopolysaccharides of gram - bacteria
  2. transport across cytoplasmic membrane is dependent upon electron transport and termed energy dependent phase 1
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9
Q

Aminoglycosides create ____ channels

A

porin

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10
Q

Aminoglycosides MOA involves

A

30s ribosome!

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11
Q

Aminoglycosides MOA (3)

A

blocks initiation of protein synthesis
blocks further translation and elicits premature termination
incorporation of incorrect amino acid

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12
Q

Variables that impact Aminoglycoside activity

A

acidic ph
anaerobic conditions
hyperosmolarity
divalent cations

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13
Q

Aminoglycoside oral absorption

A

poor IV only

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14
Q

Aminoglycoside 1/2 life

A

2-3 hours

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15
Q

Aminoglycoside elimination

A

95% renal

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16
Q

Aminoglycosides are mostly hydrophilic/hydrophobic

A

hydrophilic; does not go well into adipose tissue

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17
Q

Aminoglycosides are eliminated primarily by

A

glomerular filtration

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18
Q

Aminoglycosides are basic/acidic

A

basic

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19
Q

Aminoglycosides have ____ protein binding

A

low

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20
Q

Aminoglycosides penetration into tissues

A

bone
synovial fluid
urine (100x serum)

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21
Q

Aminoglycosides poor penetration into

A 
bronchial secretions
CNS even when inflamed
eye
bile
prostate
purulent fluids
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22
Q

Aminoglycosides have ____ elimination

A

tri-phasic

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23
Q

Aminoglycoside alpha phase (5-15min)

A

distribution of drug from blood to tissues

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24
Q

Aminoglycoside beta phase (2-4hr)

A

elimination of drug through the kidneys

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25
Q

Aminoglycoside gamme phase (150-200hr)

A

very slow release of drug from tissue binding sites concentration not detectable

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26
Q

Aminoglycosides have ____ dependent killing

A

concentration

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27
Q

Aminoglycoside PK/PD parameters

A

Cmax/MIC ratio or AUC:MIC ratio

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28
Q

Aminoglycoside Cmax:MIC preferred

A

8-10

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29
Q

Aminoglycoside dosing regimens

A

conventional and one daily

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30
Q

ODA peak mcg/ml

A

8-10 x MIC

31
Q

ODA trough mcg/ml

A

<1

32
Q

Aminoglycosides have a _____ effect even after below MIC concentrations

A

post antibiotic

33
Q

Aminoglycosides spectrum coverage

A

light purple: streptococcus, viridans, MSSA, MRSA, e. faecalis, e. faecium
dark red: h. influenzae, m. catarrhalis, E. coli, klebsiella, p. mirabilis, morganella, enterobacter, citrobacter, serratia, p. aeruginosa, acinetobacter
Misc: synergy for all gram + with cell wall active agent, active against mycobacteria, not active against steno

34
Q

Aminoglycosides are usually given ____ for gram + and usually for endocarditis

A

synergistically

35
Q

Aminoglycosides used outside of UTI for gram - infections

A

synergistically also

36
Q

Aminoglycosides are used as

_______ for gram - UTI

A

mono therapy

37
Q

Aminoglycosides mechanism of resistance

A

-enzyme modification is most common and plasmid mediated, do not confer resistance to all AG’s
-decreased uptake through altered transport or impermeable membrane or efflux, cross resistant to all AG’s and chromosomally mediated
-altered ribosome binding
streptomycin requires 1 mutation, other AGs require multiple

38
Q

Aminoglycosides adverse effects

A

ototoxicity (irreversible)
nephrotoxicity
neuromuscular blockade (Ca2+ channels)

39
Q

Aminoglycosides nephrotoxicity is called

A

non-oliguric renal failure (continues to produce urine)

40
Q

There is a ____ rise in serum creatinine with Aminoglycoside nephrotoxicity

A

slow

41
Q

A small portion of the dose is retained in the ____ lining the proximal tubules after glomerular filtration (Aminoglycoside nephrotoxicity)

A

epithelial cells

42
Q

After several days of therapy, the AGs induce characteristic _____ of proximal tubular cells consistent with the accumulation of _____.

A

changes in lysosomes; myeloid bodies

43
Q

Clincally changes in in/out occur

_____ increase serum creatinine

A

prior to

44
Q

Can also consider ____ as sign of renal damage

A

proteinuria

45
Q

Aminoglycoside ototoxicity interferes with

A

hearing (auditory) and balance (vestibular)

46
Q

Rate of occurrence of Aminoglycoside ototoxicity is about

A

<10%

47
Q

Aminoglycoside ototoxicity occurs due to direct toxic effect on ______ within the inner ear

A

hair cells

48
Q

Aminoglycoside ototoxicity can occur with _____ dosing and _____ therapy

A

conventional or QD; during or after

49
Q

There is ___ safe dose

A

NO

50
Q

Aminoglycoside ototoxicity has ____ correlation with ____ concentrations, but increased risk with sustained high troughs

A

no; peak and trough

51
Q

Serum AG levels have _______ relationship to levels within the inner ear

A

no absolute

52
Q

Aminoglycoside vestibulotoxicity is usually _____ although most patients can compensate with visual cues to maintain balance

A

irreversible

53
Q

Vestibulotoxicity symptoms include

A 
disequilibrium
ataxia
stumbling
dizziness
loss of balance
oscillopsia
N/V
vertigo
nystagmus
54
Q

Which AG is the most vestibulotoxic?

A

gentamicin

55
Q

auditory toxicity results in ___ and _____ frequency hearing loss and is _____

A

high and low; irreversible

56
Q

Which frequency hearing loss occurs first?

A

high but may not be recognized clinically

57
Q

AG are RARELY used as

A

monotherapy

58
Q

AG are usually used in combination to

A

broader coverage

59
Q

Plazomicin is a

A

semisynthetic compound

60
Q

Plazomicin is derived from

A

sisomycin

61
Q

The structure of sisomycin was modified to plazomicin in order to

A

prevent alterations by AG modifying enzymes

62
Q

Plazomicin has improved in-vitro activity against

A

aminoglycoside-resistant enterobacteriaceae

63
Q

Plazomicin structure allows it to be potent against enterobacteriaceae including

A

ESBL
AG resistant isolates
carbapenem resistant enterobacteriaceae

64
Q

Plazomicin maintains AG characteristics like

A

inhibits bacterial protein synthesis
rapid concentration-dependent activity
prolonged post-antibiotic effect

65
Q

Plazomicin oral absorption

A

poor IV only

66
Q

Plazomicin 1/2 life

A

3.5 hours

67
Q

Plazomicin elimination

A

90% renal

68
Q

Plazomicin spectrum coverage

A

light purple: MSSA, MRSA

dark red: h. influenzae, m. catarrhalis, E. coli, klebsiella, p. mirabilis, morganella, enterobacter, citrobacter, serratia

light red: p. aeruginosa, acinetobacter

Misc: active against gram - with gentamicin resistance especially carbapenemase producing KPC
not active against steno
poor activity against gentamicin resistant pseudomonas

69
Q

AG (including Plazomicin) dosing: which body weight to do you use when TBW is >25% of IBW?

A

ABW

70
Q

For AG (including Plazomicin) is renal adjustment necessary?

A

YES

71
Q

Adverse effects for Plazomicin

A 
nephrotoxocity, may be concentrated dependent
ototoxicity is assumed to be class effect but not seen in in clinical trials
72
Q

Aminoglycosides are bactericidal/bacteristatic

A

bactericidal

73
Q

The MIC of a pathogen is 2mcg/ml. What peak concentration of tobramycin should be targeted for maximal efficacy?

a. 3mcg/ml
b. 6mcg/ml
c. 12mcg/ml
d. 16mcg/ml

A

d

PC2 (18 decks)

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