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what was the first AG? What is it used for today?
streptomycin (1944)

Mycobacterium tuberculosis & alternative in gentamicin resistance
How is neomycin used today?
as a topical cream, ointment, eyedrop

Orally only for hepatic encephalopathy or gut decontamination

Not used systemically often due to increase chances for nephrotoxicity
what is kanamycin typically used for?
in the OR to clean wounds (topical irrigation solutions)

also, orally for gut decontamination
What are the three most common AGs? How are they typiaclly prescribed?
tobramycin, gentamicin, amikacin

in combination with a beta-lactam or vancomycin
explain AG killing
bactericidal/ concentration dependent with PAE
AG: MOA
bind to 30S ribosome to inhibit translation
AG is molecularly [ stable/ unstable ] and highly [nonpolar / polar ]
stable & polar (even at changes in temperature and pH (gastric acid!)
what preg catergory are AGs?
D
are AGs used in children and neonates?
yes
PAE is dependent on 3 factors. What are they?
1. drug concentration
2. amount of inoculum
3. type of organism
What routes of administration are avanilable for AGs?
IV
IM
inhalation
pleural/peritoneal= NOT RECOMMENDED
oral= absorption is not good, so i don't think it's available
explain the distribution of AGs
think about molecule: VERY POLAR

good distribution into plasma and interstitial fluids
poor into bronchial secretions, BBB, blood-CSF,biliary tract, fat/tissues bone
eye- varies depending on route of admin

**pretty much confined to plasma and interstitial fluid
explain metabolism of AGs
NOT METABOLIZED!!
**eliminated 100% unchanges in the the urine via glomerular filtration
explain the excretion of AGS
NOT METABOLIZED!!
**eliminated 100% unchanges in the the urine via glomerular filtration
Are AGs highly protein bound?
NO! Thats why they are significantly removed by dialysis
How are AGs affected by dialysis?
They are significantly removed by dialysis (becuase only 10% protein bound)
what is the half life like for AGs?
in serum 2-4 H
in otic fluid 10- 40 H
in kidney tubules 48-200 H
what is the Vd of AGs?
0.3 L/kg *use ABW
What is the formula for the peak concentration?
peak concentration = Dose / Vd
Name 3 adverse reactions of AGs
1. nephrotoxicity
2. ototoxicity
3. neuromuscular blockade
How common is nephrotoxicity with AGs?
0-50%
True or false. AG-associated nephrotixicity is reversible.
True to a certain extent
What are some risk factors for nephrotoxicity?
peak-related, elderly, concurrent nephrotoxins, pre-existing renal dz, duration and frequency (potential for accumulation)
Which drug(s) are most commonly associated with AG-induced cochlear ototoxicity?

Which drug(s) are most commonly associated with AG-induced vestibular ototoxicity?
Amikacin

Streptomycin/gentamicin
True or false. The hearing loss experienced with AGs is often reversible
false. often irreversible
NM blockade is most commone with which AG?
neomycin (IV) *which is another reason we don't use it IV (that and nephrotoxicity))


or any other AG in combo with NM-blockers
Explain the antimicrobial spectrum for AG
aMEMAglycoCIDEs
*Mema Says Please No Meat

MEMA: pseudoMEMAs (pseudomonas & other gram neg bacilli- but not stenotrophomonas maltophilia bc she would never move to FL)

SAYS: synergy with beta-lactams (staph, strep, enterococci [controversial])

PLEASE: protozoan

NO: Neisseria gonorrhoeae (gram - diplococci)

MEAT: mycobacterium (MAC and other non-tuberculosis mycobacterium= amikacin; M/tuberculosis= streptomycin)

because AGs have intrinsic resistance against HEALS
H: Haemophilus
E: enterococci
A: anaerobes
L: legionella
S; stenotrophomonas maltophilia
Name 4 ways that bacteria acquire resistance to AGs
1. aminoglycoside-inactivating enzyme (amikacin is strongest against this)
2. methylation of 30S ribosomal target
3. efflux pumps
4. biofilm production (S. aureus)
AGs are usually used in combination with ____________. When might they be used alone?
a cell-wall active agent

for a multi-drug resistant UTI
Name some infections that AGs would NOT be used for (hint: think about Vd)
osteomyelitis, meningitis

(very polar, so will not pass BBB or into bone)
which two AGs are most potent against pseudomonas?
TAP!

Tobramycin
Amikacin
Pseudomonas
When might you consider an AG via inhalation route?
cystic fibrosis patients or ventilator-associated pneumonia
Drug interactions with AGs?
TCNs and 50S agents (macrolides, lincosamides, chloramphenicol, streptogramins)

other ototoxic or nephrotoxic agents
What is conventional dosing for AGs?
q 8-12 H *but this is associated with nephrotoxicity
What is the extended interval for AG dosing?
huge dose once a day

gentamicin/tobramycin 7mg/kg

amikacin 15 mg/kg

gentamicin (gram + syngergy dose = 3mg/kg)
what should an AG trough level be? When should it be taken?
trough should be 0!
Need a drug-free interval (at least 2 H, ideally 6 H drug-free interval)

Should be taken 6-12 h after administration