Antibiotics: Nursing Pharmacology Study Guide

These agents come from living microorganisms, synthetic manufacturing, and genetic engineering, and they inhibit specific bacteria. They are bacteriostatic, bactericidal, or both. The major classes are aminoglycosides, penicillins and penicillinase-resistant drugs, sulfonamides, tetracyclines, and antimycobacterials (antitubercular and leprostatic). Others include ketolides, lincosamides, lipoglycopeptides, macrolides, and monobactams.

When bacteria invade through the respiratory tract, GI tract, or skin, the immune response produces the classic signs of inflammation (swelling, heat, redness, pain), plus fever and lethargy. Culture and sensitivity at the infection site, drawn before the first dose whenever possible, is what tells you the drug is the right one.

Antibiotics: Generic and Brand Names

Here is a table of commonly encountered antibiotics, their generic names, and brand names:

• Aminoglycosides
• amikacin (Amikin)
• gentamicin (Garamycin)
• kanamycin (Kantrex)
• neomycin (Mycifradin)
• streptomycin
• tobramycin (TOBI, Tobrex)
• Carbapenems
• doripenem (Doribax)
• ertapenem (Invanz)
• Imipenem-cilastatin (Primaxin)
• meropenem (Merrem IV)
• Cephalosporins
• First-Generation Celphalosporins
• cefadroxil
• cefazolin (Zolicef)
• cephalexin (Keflex)
• Second-Generation Cephalosporins
• cefaclor (Ceclor)
• cefoxitin
• cefprozil
• cefuroxime (Zinacef)
• Third-Generation Cephalosporins
• Cefdinir
• cefotaxime (Claforan)
• cefpodoxime (Vantin)
• ceftazidime (Ceptaz, Tazicef)
• Ceftibuten (Cedax)
• Ceftizoxime (Cefizox)
• Ceftriaxone (Rocephin)
• Fourth-Generation Cephalosporins
• cefditoren (Spectracef)
• cefepime (Maxipime)
• ceftaroline (Teflaro)
• Fluoroquinolones
• Ciprofloxacin (Cipro)
• gemifloxacin (Factive)
• levofloxacin (Levaquin)
• moxifloxacin (Avelox)
• norfloxacin (Noroxin)
• ofloxacin (Floxin, Ocuflox)
• Penicillins and Penicillinase-Resistant Antibiotics
• Penicillins
• penicillin G benzathine (Bicillin, Parmapen)
• penicillin G potassium (Pfizerpen)
• penicillin G procaine (Wycilllin)
• penicillin V (Veetids)
• Extended-Spectrum Penicillins
• amoxicillin (Amoxil, Trimox)
• ampicillin (Principen)
• Penicillinase-Resistant Antibiotics
• nafcillin
• oxacillin
• Sulfonamides
• sulfadiazine
• sulfasalazine (Azulfidine)
• cotrimoxazole (Septra, Bactrim)
• Tetracyclines
• demeclocycline (Declomycin)
• doxycycline (Doryx, Periostat)
• minocycline (Minocin)
• tetracycline (Sumycin)
• Antimycobacterials
• Antituberculosis
• First-line Antituberculotic Drugs
• ethambutol (Myambutol)
• pyrazinamide (Nydrazid)
• rifampin
• rifapentine (Rifadin, Rimactane)
• streptomycin
• Second-line Antituberculotic Drugs
• cycloserine (Seromycin)
• ethionamide (Trecator-SC)
• rifabutin (Mycobutin)
• Leprostatics
• Dapsone
• Other Antibiotics
• Ketolides
• telithromycin (Ketek)
• Lincosamides
• clindamycin (Cleocin)
• lincomycin (Lincocin)
• Lipoglycopeptides
• telavancin (Vibativ)
• Macrolides
• azithromycin (Zithromax)
• clarithromycin (Biaxin)
• erythromycin (Ery-Tab)
• Monobactams
• aztreonam (Azactam)

Antibiotics across age groups

These cautions apply across classes. Children are very sensitive to GI and CNS effects. Watch their nutrition and hydration, because oral candidiasis as a superinfection makes eating and drinking hard. Fluoroquinolones damage developing cartilage and are not recommended for growing children, and every pediatric dose gets double-checked. Teach parents to cut the unnecessary antibiotic use that drives resistance.

Adults reach for antibiotics for everything, so teach that these drugs work only against specific bacteria, not viral problems like the common cold. Tell them not to stockpile leftover pills and not to share with symptomatic friends. In older adults, assess the problem and obtain culture specimens before treating, since this group is more susceptible to adverse effects.

Aminoglycosides

Aminoglycosides treat infections caused by gram-negative aerobic bacilli. Newer, less-toxic drugs have replaced them for less serious infections because their adverse effects are potentially serious. They are bactericidal: they bind a unit of the bacterial ribosome and cause misreading of the genetic code, which kills the cell.

Use them against susceptible strains (Pseudomonas aeruginosa, Escherichia coli, Proteus spp., Klebsiella-Enterobacter-Serratia group, Citrobacter spp., Staphylococcus spp.) and for serious infections susceptible to penicillin when penicillin is contraindicated.

Pharmacokinetics

Here are the characteristic interactions of aminoglycosides and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known aminoglycoside allergy. Renal or hepatic disease can be worsened and interferes with metabolism and excretion. Preexisting hearing loss can intensify because the drug is toxic to the auditory nerve. Active herpes or mycobacterial infection can worsen because the drug blunts normal defenses. Myasthenia gravis and parkinsonism can be exacerbated by effects on the nervous system. Aminoglycosides cross into breast milk and can seriously affect a nursing infant. Amikacin should not be used longer than 7 to 10 days because it is particularly toxic to bone marrow, kidneys, and GI. Streptomycin is reserved for special situations because it is very toxic to the 8th cranial nerve and kidney.

Adverse Effects

CNS: ototoxicity, irreversible deafness, vestibular paralysis, confusion, depression, disorientation, numbness, tingling, weakness. Renal failure. Hematologic: bone marrow depression leading to immunosuppression and superinfection. GI: nausea, vomiting, diarrhea, weight loss, stomatitis, hepatotoxicity. CV: palpitations, hypotension, hypertension. Hypersensitivity: purpura, rash, urticaria, exfoliative dermatitis.

Interactions

Penicillins, cephalosporins, and ticarcillin give a synergistic bactericidal effect. Diuretics increase ototoxicity, nephrotoxicity, and neurotoxicity. Anesthetics, nondepolarizing NM blockers, succinylcholine, and citrate-anticoagulated blood increase neuromuscular blockade with paralysis.

Carbapenems

Carbapenems are a relatively new broad-spectrum class effective against gram-positive and gram-negative bacteria. They are bactericidal, inhibiting cell membrane synthesis to kill the cell.

Use them for serious intra-abdominal, urinary tract, skin and skin-structure, bone and joint, and gynecological infections, and for susceptible strains (S. pneumoniae, H. influenzae, E. coli, K. pneumoniae, B. fragilis, P. mirabilis, P. aeruginosa, P. bivia).

Pharmacokinetics

Here are the characteristic interactions of carbapenems and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known allergy to carbapenems or beta-lactams. Seizure disorders are exacerbated. Safety in meningitis is not established. It is unknown whether the drug crosses into breast milk. Ertapenem is not recommended in patients younger than 18 years. Meropenem is associated with pseudomembranous colitis and is used cautiously in inflammatory bowel disease.

Adverse Effects

GI: pseudomembranous colitis, C. difficile diarrhea, nausea, vomiting, dehydration, electrolyte imbalance. CNS: headache, dizziness, altered mental state. Superinfections.

Interactions

Carbapenems reduce serum valproic acid, which can increase seizure risk. Imipenem with ganciclovir can cause seizures. Meropenem with probenecid can drive meropenem to toxic levels.

Cephalosporins

Cephalosporins were first introduced in the 1960s. There are four generations, each with a specific spectrum, and they resemble penicillins in structure and activity. They are bactericidal and bacteriostatic, interfering with the cell wall-building ability of dividing bacteria so the wall framework cannot be synthesized.

First-generation drugs hit the same gram-positive bacteria as penicillin G plus gram-negative P. mirabilis, K. pneumoniae, and E. coli. Second-generation drugs add H. influenzae, E. aerogenes, and Neisseria spp. but are less effective against gram-positive bacteria. Third-generation drugs cover all of the above, are relatively weak against gram-positive bacteria but more potent against gram-negative bacilli including S. marcescens. Fourth-generation drugs are active against gram-negative and gram-positive organisms, including cephalosporin-resistant staphylococci and P. aeruginosa.

Pharmacokinetics

Here are the characteristic interactions of cephalosporins and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known allergy to cephalosporins or beta-lactams, since cross-reactions are common. Hepatic or renal impairment is a caution because these drugs are toxic to the kidneys and rely on them for metabolism and excretion. In pregnancy and lactation, effects on the fetus and infant are unknown; use only if benefits clearly outweigh the risk. Reserve cephalosporins for appropriate situations because resistant bacteria are appearing in increasing numbers, and perform culture and sensitivity before therapy.

Adverse Effects

GI: nausea, vomiting, diarrhea, anorexia, abdominal pain, flatulence, pseudomembranous colitis. CNS: headache, dizziness, lethargy, paresthesias. Nephrotoxicity in patients with predisposing renal insufficiency. Superinfections. Phlebitis and local abscess at IM or IV sites.

Interactions

Aminoglycosides increase nephrotoxicity risk. Oral anticoagulants increase bleeding. Avoid alcohol for 72 hours after stopping the drug to prevent a disulfiram-like reaction (flushing, throbbing headache, nausea and vomiting, chest pain, palpitations, dyspnea, syncope, vertigo, convulsions).

Fluoroquinolones

Fluoroquinolones are a relatively new synthetic class with a broad spectrum. They interfere with DNA enzymes needed for bacterial growth and reproduction. Cross-resistance is low, but short-course misuse breeds resistant strains.

Use them for respiratory, urinary tract, and skin infections caused by susceptible strains (E. coli, P. mirabilis, K. pneumoniae, P. vulgaris, M. morganii, P. aeruginosa, H. influenzae, S. aureus, S. epidermidis, N. gonorrhoeae, group D streptococci). Ciprofloxacin was approved by the FDA in August 2000 for postexposure inhalational anthrax, the first antimicrobial approved to treat an infection from a biological agent used intentionally, and it is also effective against typhoid fever.

Pharmacokinetics

Here are the characteristic interactions of fluoroquinolones and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known fluoroquinolone allergy. In pregnancy and lactation, fetal and infant effects are unknown; use only if benefits clearly outweigh the risk. Seizures can be exacerbated through effects on cell membrane channels.

Adverse Effects

GI: nausea, vomiting, diarrhea, dry mouth. CNS: headache, dizziness, insomnia, depression. Immunologic: bone marrow depression. Risk for tendinitis and tendon rupture in patients over age 60, on concurrent steroids, or with renal, heart, or lung transplants. Photosensitivity and severe skin reactions, so advise patients to avoid sun and ultraviolet light and to use protective clothing and sunscreen.

Interactions

Iron salts, sucralfate, mineral supplements, and antacids alter fluoroquinolone effect, so separate administration by at least 4 hours. Quinidine, procainamide, pentamidine, tricyclics, and phenothiazines cause severe-to-fatal cardiac reactions from increased QTc interval and torsades de pointes. Theophylline levels rise because the two share a metabolic pathway. Steroids increase CNS stimulation.

Penicillins and Penicillinase-Resistant Antibiotics

Penicillin was the first antibiotic in clinical use. Modifications followed to address resistant strains and reduce adverse effects, and penicillinase-resistant antibiotics were developed for penicillin-resistant bacteria. They are bactericidal: they block dividing bacteria from building cell walls, so the weakened wall swells and bursts under osmotic pressure.

Use them for streptococcal infections (pharyngitis, tonsillitis, scarlet fever, endocarditis) and for meningococcal meningitis at high doses.

Pharmacokinetics

Here are the characteristic interactions of penicillins and penicillinase-resistant antibiotics and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known allergy to penicillins and cephalosporins. Renal disease reduces drug excretion. In pregnancy and lactation, studies on the fetus are inadequate, and these drugs can cause diarrhea and superinfections in the infant.

Adverse Effects

GI: nausea, vomiting, diarrhea, abdominal pain, glossitis, stomatitis, gastritis, sore mouth, furry tongue. Pain and inflammation at injection sites with injectable forms. Hypersensitivity: rash, fever, wheezing, anaphylaxis with repeated exposure. Superinfections such as yeast infections.

Interactions

Tetracyclines decrease penicillin effectiveness. Parenteral aminoglycosides are inactivated.

Sulfonamides

Sulfonamides inhibit folic acid synthesis. They competitively block para-aminobenzoic acid, preventing folic acid synthesis (a precursor of RNA and DNA) in bacteria that make their own folates.

Use them against susceptible strains (C. trachomatis, Nocardia, and some strains of H. influenzae, E. coli, P. mirabilis). They are no longer used much but remain an inexpensive, effective treatment for UTIs and trachoma, especially in developing countries where cost matters, and can treat sexually transmitted diseases. Sulfasalazine treats ulcerative colitis and rheumatoid arthritis.

Pharmacokinetics

Here are the characteristic interactions of sulfonamides and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known allergy to sulfonamides, sulfonylureas, or thiazide diuretics, since cross-sensitivity occurs. Renal disease increases toxic effects. In pregnancy these drugs can cause birth defects. In lactation they raise the risk of kernicterus, diarrhea, and rash in infants.

Adverse Effects

GI: nausea, vomiting, diarrhea, abdominal pain, anorexia, stomatitis, hepatic injury. Renal: crystalluria, hematuria, proteinuria, toxic nephrosis. CNS: headache, dizziness, vertigo, ataxia, convulsions, depression. Bone marrow depression. Dermatologic: photosensitivity, rash, hypersensitivity reactions.

Interactions

Tolbutamide, tolazamide, glyburide, glipizide, and chlorpropamide increase hypoglycemia risk. Cyclosporine increases nephrotoxicity risk.

Tetracyclines

Tetracyclines are semisynthetic antibiotics based on a common soil mold. They inhibit protein synthesis so bacteria cannot multiply. Because the affected protein resembles one in human cells, they can be toxic to humans at high concentrations.

Use them against susceptible strains (Rickettsiae, M. pneumoniae, B. recurrentis, H. influenzae, H. ducreyi, Bacteroides spp., V. comma, Shigella spp., D. pneumoniae, S. aureus) and as an adjunct for protozoal infections.

Pharmacokinetics

Here are the characteristic interactions of tetracyclines and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known allergy to tetracyclines or tartrazine. In pregnancy and lactation they affect developing bones and teeth. Avoid in fungal, mycobacterial, or viral ocular infections, since ophthalmic preparations kill normal flora along with the target. Use cautiously in children below age 8 because of damage to developing bones and teeth. In hepatic or renal dysfunction, the drugs concentrate in bile and excrete in urine.

Adverse Effects

GI: nausea, vomiting, diarrhea, abdominal pain, glossitis, dysphagia, fatal hepatotoxicity. Skeletal and bones: weakened structure, staining and pitting of teeth and bones. Dermatologic: photosensitivity, rash. Superinfection. Local: pain and stinging with topical or ocular use. Hematologic: hemolytic anemia, bone marrow depression. Hypersensitivity: urticaria, anaphylaxis. Intracranial hypertension.

Interactions

Penicillin G effectiveness decreases. Oral contraceptive effectiveness decreases, so an additional birth control method is needed. Digoxin toxicity increases. Calcium, magnesium, zinc, aluminum, bismuth, and iron salts, urinary alkalinizers, and charcoal decrease tetracycline absorption.

Antimycobacterials

Antimycobacterials treat infections caused by the pathogens behind tuberculosis and leprosy. Mycobacterium tuberculosis causes tuberculosis, again the world's leading cause of death from a single infectious agent, with about 1.25 million deaths in 2023 (World Health Organization). Mycobacterium leprae causes leprosy (Hansen's disease), marked by disfiguring skin lesions and destructive effects on the respiratory tract. These drugs act on bacterial DNA and RNA, halting growth and eventually killing the organism. They are indicated for tuberculosis and leprosy.

Pharmacokinetics

Here are the characteristic interactions of antimycobacterials and the body in terms of absorption, distribution, metabolism, and excretion:

Contraindications and Cautions

Avoid in known allergy to antimycobacterials. In pregnancy there are adverse fetal effects; the safest antituberculosis regimen in pregnancy is isoniazid, ethambutol, and rifampin. Severe CNS dysfunction is exacerbated by the drug. Hepatic or renal dysfunction interferes with metabolism and excretion.

Adverse Effects

CNS: neuritis, dizziness, headache, malaise, drowsiness, hallucinations. GI: nausea, vomiting, anorexia, stomach upset, abdominal pain. Rifampin, rifabutin, and rifapentine discolor body fluids from urine to sweat to tears, may turn them orange-tinged, and can permanently stain contact lenses.

Interactions

Rifampin with INH increases toxic liver reactions. Rifampin and rifabutin with beta-blockers, corticosteroids, OCPs, oral anticoagulants, methadone, phenytoin, verapamil, ketoconazole, and cyclosporine increase metabolism and decrease effectiveness of those drugs.

Other Antibiotics

Ketolides, introduced in 2004, treat mild to moderate community-acquired pneumonia from susceptible bacteria. Lincosamides resemble macrolides but are more toxic, reserved for severe infections when penicillin or other less-toxic antibiotics cannot be used. Lipoglycopeptides, introduced in 2010, treat complicated skin and skin-structure infections from susceptible gram-positive organisms. Macrolides interfere with protein synthesis and treat respiratory infections and urethritis in adults and otitis media and pharyngitis/tonsillitis in children; erythromycin is the drug of choice for Legionnaire's disease and infections from C. diphtheriae, Ureaplasma spp., mycoplasma pneumonia, and chlamydia. Monobactams treat gram-negative enterobacterial infections.

Ketolides and lincosamides block protein synthesis to kill the cell; ketolides are structurally the same as macrolides. Lipoglycopeptides inhibit cell wall synthesis by disrupting peptidoglycan polymerization and cross-linking, binding the bacterial membrane and breaking its barrier function. Macrolides bind the bacterial cell membrane and change protein function, stopping division and causing cell death. Monobactams disrupt cell wall synthesis and promote leakage of cellular contents.

Pharmacokinetics

Here are the characteristic interactions of other antibiotics and the body in terms of absorption, distribution, metabolism, and excretion:

Ketolides

Lincosamides

Lipoglycopeptides

Macrolides

Monobactam antibiotics

Contraindications and Cautions

Ketolides: telithromycin with antiarrhythmics and antilipidemics can cause serious adverse effects and potentially fatal respiratory failure in myasthenia gravis. Lincosamides: use cautiously with hepatorenal insufficiency; in pregnancy and lactation only if the benefit clearly outweighs the risk, which also holds for lipoglycopeptides, macrolides, and monobactams.

Adverse Effects

GI: nausea, vomiting, potential pseudomembranous colitis, superinfections, taste alterations, risk for C. difficile diarrhea.

Interactions

Ketolides: loss of effect with rifampin, phenytoin, carbamazepine, or phenobarbital; increased serum digoxin and metoprolol; increased GI toxicity with theophylline. Lipoglycopeptides: increased risk for prolonged QT interval with other QT-prolonging drugs. Macrolides: food decreases absorption of oral macrolides, so take on an empty stomach with a full 8-oz glass of water 1 hour before or at least 2 to 3 hours after meals. Monobactams: incompatible in solution with nafcillin, cephradine, and metronidazole.

Nursing Considerations for Antibiotics

Assess for the cautions and contraindications above (drug allergies, CNS depression, CV disorders) before starting. Take a thorough history and exam covering other medications, CNS status, skin, respirations, and baseline labs such as renal function tests and CBC, both to establish a baseline and to catch adverse effects. Draw culture and sensitivity at the infection site so the drug matches the organism. With aminoglycosides, add orientation, reflex, and auditory testing to track CNS effects.

Likely nursing diagnoses include acute pain from GI or CNS effects, deficient fluid volume and imbalanced nutrition from diarrhea, disturbed auditory sensory perception from CNS effects, and risk for infection from bone marrow suppression (aminoglycosides) or repeated injections (cephalosporins).

Check culture and sensitivity reports to confirm the drug of choice. Give the full course as prescribed, divided around the clock, to keep levels effective and limit resistant strains. Monitor the infection site and presenting signs throughout therapy, because failure to resolve may mean you need to reculture. Provide safety measures if CNS effects (confusion, disorientation, numbness) appear. Teach the patient to change positions slowly, avoid hazardous tasks, drink plenty of fluids, keep up nutrition through nausea and vomiting, and report difficulty breathing, severe headache, fever, diarrhea, or signs of infection.

To evaluate, track the patient's response (declining signs and symptoms of infection), watch for adverse effects (orientation and affect, hearing changes, bone marrow suppression, renal toxicity, hepatic dysfunction), confirm understanding by having the patient name the drug, its indication, and adverse effects to watch for, and monitor compliance.

Frequently Asked Questions

Do antibiotics work against viruses like the common cold or flu? No. Antibiotics act only on bacteria. Taking them for a viral illness does nothing for the infection and adds to the resistance problem, so teach patients not to demand or save antibiotics for colds.

Why is it important to finish the full course of antibiotics? Stopping early can leave the hardiest bacteria alive to multiply, which drives resistant strains and can let the infection rebound. Give doses around the clock as prescribed to keep blood levels effective.

What is a culture and sensitivity test, and why draw it before the first dose? It identifies the organism and shows which antibiotics will kill it. Drawing the specimen before the first dose, whenever possible, keeps the antibiotic from skewing the result so the drug can be matched to the bug.

How serious is antibiotic resistance? Serious. The CDC estimates more than 2.8 million antimicrobial-resistant infections and more than 35,000 deaths in the United States each year (CDC, 2019). Appropriate prescribing, full courses, and not sharing or stockpiling pills all help slow it.

What major adverse effects should the nurse watch for across antibiotic classes? Allergic and anaphylactic reactions (especially penicillins and cephalosporins), C. difficile and pseudomembranous colitis, superinfections such as oral or vaginal yeast, aminoglycoside ototoxicity and nephrotoxicity, and fluoroquinolone tendon rupture and QT prolongation.

Why must some antibiotics be separated from antacids, dairy, or mineral supplements? Calcium, magnesium, aluminum, iron, and zinc bind tetracyclines and fluoroquinolones in the gut and block their absorption. Separate these drugs from antacids and mineral or dairy products by at least 2 to 4 hours.