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Cell wall inhibitors

bacterial cell wall inhibitors 1-Narrow spectrum Penicillin G&V , Anti-staphylococcal Penicillins (Oxacillin, Nafcillin), 1st generation Cephalosporins & Aztreonam
2-Moderately broad Amin-openicillin(Ampicillin), Anti-pseudomonal Penicillins (Pipracillin , Ticarcillin) , 2nd generation Cephalosporins
3-Broad spectrum: Amin-openicillin + ß-lactamase inhibitors (Ampicillin + sulbactam), 3rd & 4th generation Cephalosporins
4-Very broad spectrum: Anti-pseudomonal +ß-lactamase inhibitors (Pipracillin+ tazobactam > Ticarcillin+ clavulanate), Carbapenems (Imipenem+ Cilastatin & Meropenem)
Penicillins contain ß-lactam ring are derivatives of 6-aminopenicillanic acid
Modifications of R-group side-chain attached to ß-lactam ring.. → differences in the pharmacokinetic properties &antimicrobial spectrum of activity → Resistance to hydrolysis by enzymatic ß-lactamase →Susceptibility or stability against gastric acid
Pharmacokinetics of Penicillins: → Oral administration depending on their gastric acid stability (acid-resistance) Acid-resistant Penicillins →given orally→ PenicillinV Acid-sensitive Penicillins →given IV → PenicillinG 30 minutes before or 2-3 hours after meal
Distribution of penicillin well distributed in body fluids , lipid-insoluble → don’t enter tissue cells & poor/no penetration into CSF, unless inflammation is present (meningitis)
Elimination excreted unchanged in urine→ mainly by active tubular excretion (> 90% ) except anti-staphylococcal class (Nafcillin) → metabolized in the liver → can be given in renal failure (RF)
How does Probencid ↑ T1/2 of penicillinG!!! It blocks the active renal secretion of penicillin ...↓ the frequency of penicillin administration & prolong it’s action
Mechanism of action of Penicillins: ..Binding of the drug → “PBPs” located on the bacterial inner membrane ..inactivation of the bacterial transpeptidation reaction prevent cross-linked of “peptidoglycan chain 3- Activation of autolytic enzymes
Resistance to Penicillins: Inactivation of antibiotic with β-lactamase Modification of target PBPs Impaired penetration of drug to target PBPs Presence of efflux pump Peptidoglycan Porins
P.aeruginosa is intrinsically resistant to many antibiotics……Why -highly selective porins -produces multiple efflux pumps -ß-lactamase → amino- penicillins & most Cephalosporins are ineffective against this bacterium
[Penicillinase-enzyme is the most common & most important mechanism of resistance of ß-lactam antibiotics]
ß-lactamses-inhibitors : Structurally related to penicillin Amoxicillin/clavulanic acid, Ampicillin/sulbactam,piperacillin/tazobactam no antimicrobial properties irreversibly inhibits ß-lactamse- producing organisms ↑the activity of ß-lactams & extend their usefulness
Created by: ahmad445