Penicillin therapeutic action

Mectianism of Action A diagnostic agent that invokes immunoglobulin E which produces type I accelerated urticarial reactions to penicillins. Therapeutic Effect A positive reaction will suggest penicillin sensitivity. 

Mechanism of Action An antigout agent that competitively inhibits reabsorption of uric acid at the proximal convoluted tubule. Also, inhibits renal tubular secretion of weak organic acids, such as penicillins. Therapeutic Effect Promotes uric acid excretion, reduces serum uric acid level, and increases plasma levels of penicillins and cephalosporins. 

Mechanism of Action A penicillin that inhibits bacterial cell wall synthesis. Therapeutic Effect Bactericidal in susceptible microorganisms. 

Mechanism of Action A fixed-combination carbapenem. Imipenem penetrates the bacterial cell membrane and binds to penicillin-binding proteins, inhibiting cell wall synthesis. Cilastatin competitively inhibits the enzyme dehydropeptidase, preventing renal metabolism of imipenem. Therapeutic Effect Produces bacterial cell death. Pharmacokinetics Readily absorbed after IM administration. Protein binding 13%-21%. Widely distributed. Metabolized in the kidneys. Primarilyexcreted in urine. Removed by hemodialysis. Half-life 1 hr (increased in impaired renal function). 

Mechanism of Action A penicillin that acts as a bactericidal in susceptible microorganisms. Therapeutic Effect Inhibits bacterial cell wall synthesis. Bactericidal. Pharmacokinetics Poorly absorbed from gastrointestinal (GI) tract. Protein binding 87%-90%. Metabolized in liver. Primarily excreted in urine. Not removed by hemodialysis. Half-life 10.5-1 hr (half-life increased with imparted renal function). 

Mechanism of Action Penicillins bind to bacterial cell wall, inhibiting bacterial cell wall synthesis. Therapeutic Effect Inhibits bacterial cell wall synthesis. Beta-lacta-mase inhibitors inhibit the action of bacterial beta-lactamase. Therapeutic Effect Protects the penicillin from enzymatic degradation. 

Structural modification of an existing molecule to improve its therapeutic value, e.g., by making it more effective, less toxic, better absorbed, or longer acting (such modification can also lead to the discovery of a new pharmacologic action, as in point 2 above, or of new therapeutic effects in man, as in point 5 below). An instructive example of the major therapeutic advances that have been obtained by molecular modification is seen in the family of penicillins that followed benzyl penicillin, the original member of the series. In little more than a decade from its first characterization, the original benzyl penicillin molecule was... 

In the purposeful search that followed the demonstration of the clinical efficacy of penicillin, streptomycin was obtained from Streptomyces griseus in 1944, cultured from a heavily manured field, and also from a chicken s throat. Aminoglycosides resemble each other in their mode of action, and their pharmacokinetic, therapeutic and toxic properties. The main differences in usage reflect variation in their range of antibacterial activity crossresistance is variable. 

The penicillins, from the fungus Penicillium chryso-genum, are the oldest and most widely used antibiotics. They are formed through stepwise build-up from a tripeptide (ACV) derived from a-Amino adipic acid, cysteine, and valine. Successive oxidation steps form the p-lactam and close the thiazolidine ring to form isopenicillin N. Action of an acyltransferase then yields penicillin G (Fig. 47). Alternatively, hydrolysis of isopenicillin N (or penicillin G) yields 6-aminopenicillanic acid, a key precursor for the wide range of semisynthetic pencillins used therapeutically. 

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