Foundation University

COLLEGE OF NURSING
Dumaguete City

PHARMACOLOGY-II

Katrina Estoconing

Answer the following:

Antibacterial

1. Explain the mechanisms of action of antibacterial drugs.

• Antibacterial drugs work by targeting specific components or processes within bacterial cells, either
by killing the bacteria (bactericidal) or by inhibiting bacterial growth (bacteriostatic). There are
several different classes of antibacterial drugs, each with its own mechanism of action.
• Beta-lactams: This class of antibiotics includes penicillins, cephalosporins, and carbapenems. Beta-
lactams work by inhibiting bacterial cell wall synthesis, which leads to cell death. They do this by
binding to and inactivating enzymes called penicillin-binding proteins (PBPs), which are involved in
the cross-linking of peptidoglycan chains in the cell wall.
• Macrolides: This class of antibiotics includes erythromycin, azithromycin, and clarithromycin.
Macrolides work by inhibiting bacterial protein synthesis. They do this by binding to the 50S subunit
of bacterial ribosomes, which prevents the formation of peptide bonds between amino acids during
protein synthesis.
• Fluoroquinolones: This class of antibiotics includes ciprofloxacin, levofloxacin, and moxifloxacin.
Fluoroquinolones work by inhibiting bacterial DNA synthesis. They do this by binding to enzymes
called DNA gyrase and topoisomerase IV, which are involved in DNA replication and repair.
• Aminoglycosides: This class of antibiotics includes gentamicin, tobramycin, and amikacin.
Aminoglycosides work by inhibiting bacterial protein synthesis. They do this by binding to the 30S
subunit of bacterial ribosomes, which interferes with the initiation of protein synthesis and causes
misreading of the genetic code.

2. Differentiate between bacteria that are naturally resistant and those that have acquired resistance to an
antibiotic.
Bacteria can exhibit either intrinsic or acquired resistance to antibiotics. Naturally resistant bacteria,
also known as intrinsic resistance, are bacteria that have a natural ability to resist the effects of certain
 antibiotics. This resistance is often due to the presence of certain structural or functional characteristics that
make it difficult for the antibiotic to penetrate the bacterial cell wall or interfere with its metabolic processes.
For example, Gram-negative bacteria have an outer membrane that makes it difficult for certain antibiotics
to penetrate and reach their target site.

Acquired resistance on the other hand, occurs when bacteria that were previously susceptible to an
antibiotic develop the ability to resist its effects. This can occur through a variety of mechanisms, including
mutation or acquisition of resistance genes from other bacteria. For example, bacteria can acquire resistance
genes through horizontal gene transfer, such as through plasmids or transposons. This acquired resistance can
occur in response to antibiotic use or exposure, and can be a significant problem in healthcare settings where
antibiotics are frequently used.
3. Summarize the three general adverse effects associated with
antibacterial drugs.

• Allergic reactions - Antibacterial drugs can cause allergic reactions, ranging from mild skin rashes to severe
anaphylaxis. These reactions can occur immediately after drug administration or days to weeks later.
• Superinfection - Antibacterial drugs can also lead to superinfection, which is the development of a new
infection caused by a different microorganism that is resistant to the original antibiotic. This can occur when
the antibiotic kills off a patient's normal flora, allowing other microorganisms to overgrow and cause
infection.
• Organ toxicity - Some antibacterial drugs can cause organ toxicity, particularly to the liver and kidneys. This
can occur due to the accumulation of the drug or its metabolites in these organs, as well as due to the drug's
effects on cellular metabolism. Patients with pre-existing liver or kidney disease are particularly susceptible
to these adverse effects.

4. Differentiate between narrow-spectrum and broad-spectrum

antibiotics.

Narrow-spectrum antibiotics are effective against only a limited range of microorganisms. For example,
penicillin is a narrow-spectrum antibiotic that is primarily effective against gram-positive bacteria. These antibiotics
are often preferred when the causative organism is known or suspected, as they can help to minimize the development
of antibiotic resistance and reduce the risk of adverse effects.

Broad-spectrum antibiotics are effective against a wide range of microorganisms, including both gram-positive
and gram-negative bacteria. Examples of broad-spectrum antibiotics include tetracyclines and fluoroquinolones.
These antibiotics are often used when the causative organism is unknown or when the patient has a severe or life-
threatening infection that requires immediate treatment. However, the use of broad-spectrum antibiotics can increase
the risk of superinfection and the development of antibiotic resistance.

5. Contrast the effects of first-, second-, third-, fourth-, and fifthgeneration cephalosporins.
• First-generation cephalosporins (e.g. cephalexin): These antibiotics are primarily effective against
gram-positive bacteria, such as Streptococcus and Staphylococcus. They have limited activity against
gram-negative bacteria and are often used to treat skin and soft tissue infections.
• Second-generation cephalosporins (e.g. cefuroxime): These antibiotics have broader activity against
both gram-positive and gram-negative bacteria, including some anaerobic bacteria. They are often
used to treat respiratory and urinary tract infections.
• Third-generation cephalosporins (e.g. ceftriaxone): These antibiotics have even broader activity
against gram-negative bacteria, including Pseudomonas aeruginosa. They are often used to treat
serious infections, such as sepsis and meningitis.
• Fourth-generation cephalosporins (e.g. cefepime): These antibiotics have similar activity to third-
generation cephalosporins against gram-negative bacteria, but also have increased activity against
gram-positive bacteria. They are often used to treat complicated infections, such as hospital-acquired
pneumonia.
• Fifth-generation cephalosporins (e.g. ceftaroline): These antibiotics have activity against both gram-
positive and gram-negative bacteria, including methicillin-resistant Staphylococcus aureus (MRSA).
They are often used to treat complicated skin and soft tissue infections.

6. Describe the pharmacokinetics and pharmacodynamics of erythromycin.

Pharmacokinetics:
- Absorption: Erythromycin is well absorbed from the gastrointestinal tract, but its absorption is reduced by
food. Enteric-coated formulations can help to reduce this effect.
- Distribution: Erythromycin is widely distributed throughout the body, including into tissues and fluids such
as the lungs, skin, and bile. It can also cross the placenta and enter breast milk.
- Metabolism: Erythromycin is metabolized in the liver and excreted primarily in the bile.
- Elimination: The elimination half-life of erythromycin is approximately 2-4 hours in adults. It is excreted
primarily in the feces, with only a small amount excreted in the urine.

Pharmacodynamics:
- Mechanism of action: Erythromycin binds to the 50S ribosomal subunit of bacteria, inhibiting protein
synthesis and leading to bacterial cell death.
 - Spectrum of activity: Erythromycin is effective against a wide range of gram-positive and some gram-
negative bacteria, as well as some atypical bacteria such as Mycoplasma and Chlamydia.
- Resistance: Resistance to erythromycin can develop due to mutations in the bacterial ribosome or through
the acquisition of resistance genes.
- Dosing: Erythromycin is typically administered orally or intravenously, and dosing varies based on the
indication and patient factors such as age and weight.
- Adverse effects: Erythromycin can cause gastrointestinal upset, such as nausea, vomiting, and diarrhea. It
can also cause QT prolongation and cardiac arrhythmias, particularly in patients with pre-existing cardiac
conditions.

7. Summarize the nurse’s role in detecting ototoxicity and

nephrotoxicity associated with the administration of
aminoglycosides.

The nurse's role in detecting ototoxicity

- Assess the patient's hearing and balance before starting aminoglycoside therapy, and periodically throughout
treatment.

- Monitor for signs and symptoms of ototoxicity, such as tinnitus, vertigo, and hearing loss.

- Report any changes in hearing or balance to the healthcare provider immediately.

- Advise the patient to report any changes in hearing or balance as soon as possible.

The nurse's role in detecting nephrotoxicity

- Monitor the patient's renal function before starting aminoglycoside therapy, and periodically throughout treatment.

- Assess the patient for signs and symptoms of nephrotoxicity, such as decreased urine output, elevated serum
creatinine levels, and electrolyte imbalances.

- Report any changes in renal function to the healthcare provider immediately.

- Advise the patient to report any changes in urinary output, color, or odor as soon as possible.

8. Contrast the nursing interventions for each of the drug categories:macrolides, tetracyclines, aminoglycosides,
and fluoroquinolones.
 Macrolides:
- Assess for allergies to macrolides or other antibiotics.
- Monitor for gastrointestinal side effects such as nausea, vomiting, and diarrhea.
- Administer with food to decrease gastrointestinal side effects.
- Monitor liver function tests if the patient has liver disease.
- Monitor for signs and symptoms of QT prolongation and cardiac arrhythmias.

Tetracyclines:
- Assess for allergies to tetracyclines or other antibiotics.
- Administer on an empty stomach with a full glass of water to increase absorption.
- Avoid administering with dairy products, antacids, or iron supplements as they can decrease absorption.
- Monitor for gastrointestinal side effects such as nausea, vomiting, and diarrhea.
- Monitor for photosensitivity and advise the patient to avoid prolonged exposure to sunlight.

Aminoglycosides:
- Assess for allergies to aminoglycosides or other antibiotics.
- Monitor renal function and electrolytes as aminoglycosides can cause nephrotoxicity.
- Monitor for ototoxicity and report any changes in hearing or balance to the healthcare provider immediately.
- Monitor for signs and symptoms of neuromuscular blockade, such as respiratory depression or muscle
weakness.
- Administer through a large-bore intravenous catheter and monitor for phlebitis.

Fluoroquinolones:
- Assess for allergies to fluoroquinolones or other antibiotics.
- Monitor for gastrointestinal side effects such as nausea, vomiting, and diarrhea.
- Monitor for signs and symptoms of tendonitis or tendon rupture.
- Monitor for QT prolongation and cardiac arrhythmias.
- Advise the patient to avoid prolonged exposure to sunlight and to use sunscreen.

9. Differentiate between short-acting and intermediate-acting

sulfonamides.

Short-acting sulfonamides, such as sulfisoxazole, have a shorter half-life and require more frequent
dosing while Intermediate-acting sulfonamides, such as sulfamethoxazole, have a longer half-life and can be
given less frequently.
10. Explain the pharmacokinetics of the sulfonamides.
Sulfonamides are well absorbed from the gastrointestinal tract. They are widely distributed throughout
the body, including into tissues and fluids such as the lungs, skin, and urine. Sulfonamides are metabolized
in the liver and excreted primarily in the urine. The elimination half-life of sulfonamides varies depending
on the specific drug, but is generally around 6-12 hours in adults.

References:

Murray PR, Rosenthal KS, Pfaller MA. Medical Microbiology. 9th edition. Elsevier; 2020.

Katzung BG, Masters SB, Trevor AJ. Basic and Clinical Pharmacology. 14th edition. McGraw Hill
Education; 2018.

McCuistion, L. (2021). Pharmacology: A patient-centered nursing process approach. (10th ed.). Singapore:
Elsevier Pte Ltd.