Antibacterial Drugs General
Terminology
Antibacterials/Antimicrobials and Antibiotics
Antibacterials and antimicrobials inhibit the growth of or
kill bacteria.
Antibiotics are substances produced by a particular type of
microorganism that inhibit growth of or kill a different microorganism.
Bacteriostatic: inhibit bacterial growth.
Bactericidal: kill bacteria.
Natural or manufactured substances work with normal body
defenses and medical procedures to treat infections.
Mechanism of action:
The antibacterial prevents cell
wall synthesis of the bacteria by enzyme breakdown. Cell wall damage will cause the cell to fill
with water eventually rupturing, which kills the bacterial cell.
Inhibition of enzyme synthesis
causes the bacterial cell membrane to become more permeable causing loss of
cellular substance and cell lysis.
Protein synthesis is inhibited in
the bacteria without affecting normal cells. Protein production is needed for cell
structure and enzyme action in order for the bacteria to survive.
The antibacterial binds with
nucleic acid and enzymes required for nucleic acid synthesis to stop the
formation of ribonucleic acid (RNA) and deoxyribonucleic acid (DNA).
The antibiotic then interferes with
steps of cell metabolism.
Pharmacokinetics and Pharmacodynamics
Antibiotics have high affinity to bacterial cell wall
binding sites. Absorption, distribution,
metabolism, and excretion will over all determine how long an antibiotic is
bound to the bacterial cell wall receptor sites. The longer the half-life the
longer the drug remains on the binding sites. This means less frequent dosing.
Minimum effective concentration (MEC) is needed for an
antibacterial to be effective.
Antibiotic dosing intervals depends on pathogen type, location of the
infection, severity of the infection, and immunocompetence of the client. Peak and trough levels may be require in
drugs with a narrow therapeutic index.
Body Defenses
Client age, immunoglobulins, white blood cells (WBCs),
nutrition, organ function, and circulation will affect the body’s ability to combat
infection.
Resistance to Antibacterials
Bacterial growth continues despite use of antibacterials.
Natural or inherent resistance: no prior exposure to the
antibacterial drug being used.
Acquired resistance: prior exposure to the antibacterial
drug being used causes the bacteria to evolve and become resilient.
Bacteria evolve as minor mutations occur. Eventually the bacteria to become resistant
to antibiotics that normally killed them.
The
bacteria can produce an enzyme which will destroy an antibiotic.
The bacterial cell wall receptor
binding sites can modify so the antibiotic no longer recognizes the cell.
The bacterial cell wall can evolve
to inhibit the action of the antibiotic even if it reaches the binding sites.
The bacteria can adapt to push out
antibiotic that reaches the cell through efflux resistance, preventing adequate
MEC.
Bacteria are able to transmit genetic material to other
species of bacteria causing them to become resistant.
Methicillin-resistant-staphylococcus aureus (MRSA) is
bacteria resistant to methicillin, penicillin, and cephalosporins. Vancomycin (Vancocin) is most often used as
treatment.
Vancomycin-resistant enterococci faecium (VREF) is on the
rise and may cause death in immunocompromised clients. Linezolid (Zyvox) can be used for treatment.
Preventing further resistance
New drugs are being
developed that will disable the antibiotic resistant action in the bacteria
when taken with an antibiotic.
Studies have revealed
inappropriate use of antibiotics in 50% of hospitalized clients. Frequent and improper use of antibiotics can cause
resistance to occur more rapidly.
Culture and sensitivity (C & S) testing is done
to identify the infecting bacteria and which antibiotic will be best to kill
it.
Broad-spectrum antibiotics are effective against
gram-positive and gram-negative bacteria.
Narrow-spectrum antibiotics are
effective against a specific type of bacteria.
Assess patient for effectiveness of treatment.
Ensure peak and trough levels are drawn at correct time intervals.
Teach clients to take antibiotic until it is completely gone.
Encourage the client to increase fluid intake.
Aziz, A. (2013). The role of healthcare
strategies in controlling antibiotic resistance. British Journal Of Nursing, 22(18), 1066-1074.
Kee, J.L., Hayes, E.R., & McCuistion, L.E.
(2012). Pharmacology: A nursing process
approach. St. Louis: Elsevier Saunders.
Question: I am having some trouble understanding the mechanism of action. I am trying to keep it simple and to the point. Do you think what I have is adqeuate? Any advice is greatly appreciated.
The mechanism of action will depend on the class of antimicrobial. Some classes are bacteriocidal (kill), some are static (inhbit growth). Quinolones interfere with enzymes that re needed to make bacterial DNA. Penicillins inhibit bacterial cell wall formation of mucopeptides. Macrolides bind to ribosomal subunits to interfere with protein syntheses. There is no real easy way to explain MOA. One thing that is worth mentioning is the term Antimicrobial Stewardship. It is a concept of right drug/bug combinations for the right duration of therapy at the right dose. By decreasing broad spectrum antibiotic use, encouraging IV to oral transitions and tailoring therapy based on culture results, we can hopefully decrease adverse effects, decrease resistance and health care costs overall.
ReplyDeleteThanks so much for the feedback. It has been very helpful. I added a section on antimicrobial stewardships.
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