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Nur 243 Antibiotics and Diabetic Agents Summary

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This is a comprehensive and detailed summary on Antibiotics and Diabetic Agents from the book Pharmacology for Nursing Care by Richard A. Lehne. *Essential Study Material!!

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  • September 18, 2024
  • 32
  • 2019/2020
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Basic Principles of Antimicrobial Therapy:
Antibiotic:
→ a chemical that is produced by one microbe and has the ability to harm 
other microbes 
→ drugs such as sulfonamides that are produced in the lab are not antibiotics by
“strict” definition
→ narrow spectrum antibiotics are preferred to broad spectrum antibiotics
→ broad spectrums can be used as initial treatment then switched to narrow when
identity of bacteria is known
→ samples of exudates and body fluids must be obtained before initiation of
antibiotic treatment
→ antibiotics should not be d/c prematurely; if they are→ recurrent infection
MULTIPLE ANTIBIOTIC THERAPY→ INFECTION HAS UNKNOWN ETIOLOGY AND PT IS
NEUTROPENIC
→ in some cases antibiotic combination can reduce toxicity to the host and in some cases it
can increase toxicity
Antimicrobial Drug:
→ any agent, natural or synthetic, that has the ability to kill or suppress
microorganisms
→ no benefit/ significant diff. in the terms antimicrobial drug and antibiotic so
they’re used interchangeably
→ Antimicrobial therapy: #1 rule catch the drug with the bug
⇒ objective not to kill infecting organism, it is to suppress microbial growth to
the point at which the balance is tipped in favor of the host
→additive response→ antimicrobial effect of the combination of two drugs is equal
to the sum of effects of the two drugs alone
→ potentiative/synergistic response→ the effect of the drug combination is greater
than the sum of the effects of the two drugs alone (ex penicillin combined w/
aminoglycoside to treat enterococcal endocarditis)
→ antagonistic response→ effect is less; not significant if host defense is intact
→ common when bactericidal agent (ex penicillin) is combined with
bacteriostatic agent (ex tetracycline)
Selective toxicity:
→ the ability of a drug to injure a target cell or target organism 
without injuring other cells or organisms that are intimate contact with 
the target
→ the ability of an antibiotic to kill or suppress microbial 
pathogens without causing injury to the host
Bactericidal Drug:

,→ directly lethal to bacteria at clinical concentrations
Bacteriostatic Drug:
→ slow bacterial growth; does not cause cell death
Acquired resistance:
→ over time drug that is effective becomes useless
→ problems w c-diff, staph, enterococci, pseudomonas, acinetobacter, klebsiella
→ MICROBE becomes resistant not the patient
Superinfection:
→ a NEW secondary infection that appears during the course of a primary infection
→ develop when antibiotics eliminate the inhibitory influence of normal flora
→ example of emergence of drug resistance
DISINFECTANT→ KILL BACTERIA→ APPLY TO SURFACES AND INSTRUMENTS
ANTISEPTIC→ INHIBIT MICROORGANISMS→ APPLY TO SKIN
Bacterial Cell Wall:
-osmotic pressure w/in bacterium is high
-If not for the cell wall bacteria would absorb water and burst
-drugs that weaken cell wall (penicillin and cephalosporin) cause bacterial lysis
-mammals do not have cell walls
Sulfonamides:
-antimetabolite
-selectively toxic to specific microbes; deprives the bacteria of folic acid
-inhibit an ENZYME critical to BACTERIAL survival
→ para-aminobenzoic acid makes folic acid; humans can safely receive sulfonamides
as treatment because folic acid is received dietarily and is not produced w/in the
body→ toxicity only in microbes
→ sulfonamides block conversion of Para-Aminobenzoic Acid acid (PABA) into folic
acid
Bacterial Protein Synthesis:
-bacteria do not have identical ribosomes, unlike humans; antibiotics can impair
bacterial ribosomes leaving ribosomes of mammalian untouched
Mechanisms of Action: Drugs→
-inhibit cell wall synthesis (promote bacterial lysis and death)--> penicillin and
cephalosporin
-increase cell membrane permeability (causing leakage of intracellular material)-->
amphotericin B
-cause lethal inhibition of bacterial protein synthesis (kills bacteria)-->
aminoglycosides/gentamicin
-that cause non-lethal inhibition of bacterial protein synthesis(slow microbial growth
they do not kill them)--> tetracyclines

,-that inhibit bacterial synthesis of DNA and RNA or disrupt DNA function (bind
directly to nucleic acids or DNA/ interfere with nucleic acid synthesis)--> ciprofloxacin
-antimetabolites (disrupt biochemical reactions)--> sulfonamides
-drugs that suppress viral replication (inhibit protease, polymerase, transcriptase,
etc)
→
results from  or from acquisition of DNA from an external
source ie  -> these are independent of drug use
-Use of antibiotics promotes the emergence of drug resistant microbes
-If a drug resistant organism is present antibiotics will create selection pressure
favoring its growth by killing sensitive organisms that are not resistant to the drug
-All microbial drugs facilitate resistance, but broad spectrum facilitate the most
→ EXCEPTION=drugs to treat TB SUPPRESS RESISTANCE
-more antibiotics=faster drug resistance
-hospitals use large amount of antibiotics→ HAI’s; DIFFICULT TO TREAT
Microbial Mechanisms of Drug Resistance:
⇒ at site of action→ mostly intracellular→ microbes stop uptake of certain drugs
(gentamicin, tetracycline) or increase export of drug→ resistance
⇒ molecule structure is altered→ resistance
⇒ microbe synthesizes compound that antagonizes drug action→ resistance
Drug Inactivations
→ microbes can resist harm by producing drug metabolizing enzymes
→ penicillinase is produced to inactivate penicillin
→ New Delhi Metallo-Beta-Lactamase 1 or  gene in bacteria that codes for
extreme resistance; Inactivates drugs with beta-lactam ring (penicillin, cephalosporin);
bacteria that have gene are resistant to ALL antibiotics except colistin and tigecycline
Spontaneous Mutation
-gradual→ low level resistance develops first, greater resistance with additional
mutations; confer resistance to only 
Conjugation
-extrachromosomal DNA is transferred from one bacterium to another
-donor must possess 2 unique DNA segments
-takes place among gram negative bacteria
- resistance
→ 1 codes for the sexual apparatus required for DNA transfer
→ 1 codes for the mechanisms of drug resistance
→ the 2 combine= R Factor (resistance factor)
→ R factors are becoming common in NORMAL FLORA (resistance transfer from
normal flora to pathogen is a clinical concern)

, Selecting An Antibiotic→
1. Identity of infecting organism
a. Microscopic examination of gram stained preparation are quickest,
simplest, and most versatile
b. Samples for stain include blood, sputum, urine, and other body fluids
c. Most useful sample=direct aspirates from site of infection
d. Polymerase Chain Reaction test/ Nucleic Acid Amplification test can
detect low titers of bacteria and viruses
i. More specific and more sensitive than gram stain
2. Drug sensitivity of infecting organism
3. Host factors such as site of infection and status of host defenses
Determining Drug Susceptibility:
→ sensitivity testing is not always needed
→ indicated when resistance is common (ex staph and gram neg. bacilli)

Aka Kirby-Bauer test
Performed by seeding an agar plate with infected organism solution
and placing on plate with several paper disks that have been
impregnated with various antibiotics
The degree of drug sensitivity is proportional to the size of the bacteria
free zone

a. Bacteria are grown in a series of tubes containing direct concentrations
of an antibiotic
b. Provides more precise drug sensitivity
c. Good for est. therapy for infections very hard to treat
d. Establishes 2 clinical values

1. The lowest concentration of antibiotic that produces
complete inhibition of bacterial growth (does not kill)
2. Drug levels 4-8x the minimum inhibitory concentration is
desirable

1. The lowest concentration of drug that produces a 99.9%
decline (kills) in bacterial colonies

a. Similar to disk diffusion but finds more precise MIC
b. Uses narrow test strips instead of disk; and uses 15 concentrations of
same antibiotic instead of all different ones

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