Aminoglycosides

Aminoglycosides

Content

Aminoglycosides

       Mechanism
of action

       Pharmacokinetics

       Adverse
effects

       Clinical
uses

Objectives

At the end of this session, students will be able to:

       List
various aminoglycosides

       Describe
the mechanism of action of aminoglycosides

       Outline
the pharmacokinetics of aminoglycosides

       Explain
the clinical uses of aminoglycosides

Aminoglycosides

       Two
amino sugar aminocyclitol (non-sugar) by a glycosidic bond

       In
streptomycin, aminocyclitol is placed lateral to the aminosugar (Streptose) in
turn joined by another amino sugar (N-methyl-L-glucosamine)

       Two
amino sugars jointly called streptobiosamine

       Obtained
from genus Streptomyces

Structure of aminoglycoside

Aminoglycosides Classification

       Streptomycin

       Gentamicin

       Sisomicin

       Netilmicin

       Kanamycin

       Tobramycin

       Amikacin

       Neomycin

       Paromomycin

       Soframycin

       Spectinomycin

Aminoglycosides – Mechanism of action

       Bactericidal,
Concentration dependent killing

       Post
antibiotic effect  – dose dependent

       Drug
diffuses through outer coat of gram negative bacteria

       Aqueous
porin channels

       Reached
periplasmic space

       May
also bind to 50s ribosomal subunit

       Prevents
the formation of initiation complex

       Freezing
of protein synthesis

       Misreading
of genetic code on mRNA

       Incorporation
of incorrect aminoacids

       Loss
of cell membrane integrity

Mechanism of resistance

       Inactivation
of drug

      Plasmid
mediated acetyl transferase

      Plasmid
mediated adenyl transferase

      Plasmid
mediated phosphotransferase

       Restriction
in the entry of drug though deletion or mutation of channels

       Alteration
in the binding site

Pharmacokinetics

       Polar
cation – No absorption when given orally

       Given
parenteral (IM) or topical

       On
IM administration  – good
bioavailability, peak plasma – 30-90 mins

       Accumulates
on pleural cavity and in synovial fluid

       Metabolism  – insignificant

       In
pregnancy – accumulates in foetal plasma – hearing loss

       Excretion
– Kidney

Antimicrobial spectrum

Narrow spectrum – effective against gram positive bacteria

       Shigella

       Proteus

       Enterobacter

       Pseudomonas
aeruginosa

       Klebsiella

       Serratia

Adverse effects

        Renal
toxicity – reversible

       Accumulation
in kidney

       Degranulation
of lysosome

       Release
of acid hydrolase

       Digestion
of cell organelles

       Digested
organelles are sloughed off

       Excreted
in urine

        Ototoxicity

       Accumulates
in perilymph and endolymph

       Damage
to VIII cranial nerve

       Vestibular
toxicity – by streptomycin and gentamycin

      Ataxia

      Loss
of body balance

       Cochlear
toxicity – Neomycin and amykacin

      Hearing
difficulties

      Tinnitus

        Neuro-muscular
blockade – during

       Deplacement
of calcium from neuromuscular junction

       Inhibition
of ach release

       Calcium
gluconate as i.v injection

       AchE
inhibitors

Clinical uses

       Streptomycin
– TB, plague, tularemia, Bacterial endocarditis

       Many
aminoglycosides are combined with penicillin and cephalosporins

       UTI,
hospital acquired pneumonia, osteomylitis, meningitis, peritonitis, burns and
otitis

Summary

       Aminoglycosides
consists of two amino sugar joined by aminocyclitol (non-sugar) by a glycosidic
bond

       They
act by inhibiting protein synthesis by binding to 30s and sometime 50s
ribosomal subunits

       Inhibited
by divalent cations

       Resistance
develops early

       Used
in TB, tularemia, bacterial endocarditis, UTI

       Associated
adverse effects like ototoxicity, renal toxicity and neuro muscular blockade

 

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