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What is the mechanism of action of penicillins?
Answer: They bind penicillin-binding proteins (PBPs) and inhibit bacterial cell wall synthesis, causing cell lysis (bactericidal).
Effective mainly against actively dividing, gram-positive organisms because the cell wall target is most vulnerable during growth.
What infections are penicillins used to treat, and what is a classic drug/indication pairing?
Answer: Gram-positive infections (strep throat, pneumonia), and penicillin G/benzathine penicillin is first-line for syphilis.
What is the signature adverse effect of penicillins and the nursing priority?
Answer: Hypersensitivity reaction, including anaphylaxis; assess for allergy history before administration and have emergency equipment available.
Patients with a severe penicillin allergy have an increased (though not universal) risk of cross-reactivity with cephalosporins.
Penicillin patient teaching points
Answer: Complete the full course even if feeling better; take with water (some need empty stomach, amoxicillin can be taken with food); report rash, hives, or difficulty breathing immediately.
Probenecid can be given with penicillin to prolong its action by blocking renal excretion.
Mechanism of action of cephalosporins
Answer: Beta-lactam antibiotics that inhibit bacterial cell wall synthesis by binding PBPs, similar to penicillins (bactericidal).
Divided into 1st–5th generations based on spectrum of activity.
General trend across cephalosporin generations (1st to 4th/5th)?
Answer: As generation increases, gram-negative coverage increases and CNS penetration improves; gram-positive coverage generally decreases (except 5th gen, which regains MRSA coverage).
1st generation cephalosporin example and common use
Answer: Cefazolin — used mainly for gram-positive coverage and surgical prophylaxis.
2nd generation cephalosporin example and use
Answer: Cefuroxime — expanded gram-negative coverage compared to 1st generation, used for respiratory and sinus infections.
3rd generation cephalosporin example and notable feature
Answer: Ceftriaxone — broad gram-negative coverage with good CNS penetration, used for meningitis and gonorrhea.
4th generation cephalosporin example and use
Answer: Cefepime — very broad spectrum including Pseudomonas aeruginosa, used for serious/hospital-acquired infections.
5th generation cephalosporin example and unique coverage
Answer: Ceftaroline — broad spectrum that also covers MRSA, unlike earlier generations.
What special interaction do some cephalosporins (e.g., cefotetan) have with alcohol?
Answer: A disulfiram-like reaction (flushing, nausea, vomiting, headache) if alcohol is consumed.
Teach patients to avoid alcohol during and for several days after therapy with these specific agents.
Mechanism and spectrum of carbapenems (e.g., imipenem, meropenem)
Answer: Beta-lactams that inhibit cell wall synthesis; have the broadest spectrum of antibacterial activity, used for severe/multidrug-resistant infections.
Often reserved as last-line agents to limit resistance development.
Signature adverse effect of carbapenems, especially imipenem
Answer: Increased seizure risk, particularly in patients with renal impairment or CNS disorders; requires renal dose adjustment.
Mechanism of action and uses of vancomycin
Answer: Inhibits bacterial cell wall synthesis at a different site than beta-lactams; used IV for serious MRSA infections and orally for C. difficile colitis.
Oral vancomycin is not absorbed systemically, so it acts locally in the GI tract for C. diff.
What is Red Man Syndrome and how is it prevented?
Answer: A histamine-mediated reaction (flushing, rash, itching of face/neck/trunk, hypotension) caused by rapid IV vancomycin infusion; prevented by infusing slowly over at least 60 minutes.
Not a true allergy — it's related to infusion rate, not IgE-mediated hypersensitivity.
What labs/monitoring are required with IV vancomycin?
Answer: Trough drug levels, renal function (BUN/creatinine), and signs of ototoxicity (hearing changes, tinnitus).
Vancomycin is nephrotoxic and ototoxic, especially with prolonged use or concurrent nephrotoxic drugs.
Mechanism of action of aminoglycosides
Answer: Bind the bacterial 30S ribosomal subunit, inhibiting protein synthesis; bactericidal, primarily active against aerobic gram-negative bacteria.
Examples: gentamicin, tobramycin, amikacin.
Signature adverse effects of aminoglycosides
Answer: Ototoxicity (hearing loss, tinnitus, vertigo) and nephrotoxicity.
Risk increases with prolonged therapy, high doses, renal impairment, and concurrent nephrotoxic/ototoxic drugs (e.g., loop diuretics, vancomycin).
What monitoring is essential with aminoglycoside therapy?
Answer: Peak and trough serum drug levels, renal function tests (BUN/creatinine), and hearing assessment.
Peak levels assess efficacy; trough levels assess toxicity risk.
Mechanism of action of macrolides (e.g., azithromycin, erythromycin)
Answer: Bind the 50S ribosomal subunit, inhibiting bacterial protein synthesis; typically bacteriostatic.
Often used as an alternative for patients with penicillin allergy, and for atypical pneumonia (Mycoplasma, Legionella, Chlamydia).
Signature adverse effects of macrolides
Answer: GI upset (especially erythromycin), QT prolongation/risk of dysrhythmias, and hepatotoxicity.
Key drug interaction concern with macrolides
Answer: They inhibit the CYP3A4 enzyme, increasing levels/toxicity of drugs like warfarin, statins, and theophylline.
Mechanism of action of tetracyclines
Answer: Bind the 30S ribosomal subunit, inhibiting bacterial protein synthesis; bacteriostatic, broad spectrum.
Examples: doxycycline, tetracycline, minocycline.
Signature adverse effects of tetracyclines
Answer: Photosensitivity, tooth discoloration and inhibited bone growth in children, and GI upset.
Contraindicated in pregnancy and in children under 8 due to effects on developing teeth and bones.
Tetracycline patient teaching points
Answer: Avoid dairy products, antacids, and iron supplements (they chelate the drug and reduce absorption); use sunscreen and avoid prolonged sun exposure; take on an empty stomach when possible.
Mechanism of action of fluoroquinolones (e.g., ciprofloxacin, levofloxacin)
Answer: Inhibit bacterial DNA gyrase and topoisomerase IV, preventing DNA replication; bactericidal.
Signature black-box adverse effect of fluoroquinolones
Answer: Tendinitis and tendon rupture (especially Achilles tendon), risk increased in older adults and with concurrent corticosteroid use.
Teach patients to stop the drug and report tendon pain/swelling immediately.
Other notable adverse effects of fluoroquinolones
Answer: QT prolongation, CNS effects (dizziness, seizures), photosensitivity, and peripheral neuropathy.
Avoid in children and pregnant women due to effects on developing cartilage.
Fluoroquinolone patient teaching regarding administration
Answer: Avoid taking with dairy products, antacids, iron, or calcium/magnesium supplements, which impair absorption; use sun protection.
Mechanism of action of sulfonamides (e.g., sulfamethoxazole-trimethoprim)
Answer: Inhibit folic acid synthesis by competing with PABA, impairing bacterial DNA synthesis.
Trimethoprim-sulfamethoxazole (Bactrim) blocks two sequential steps in folate synthesis, giving synergistic bactericidal effect.
Signature adverse effects of sulfonamides
Answer: Stevens-Johnson syndrome, sulfa allergy (cross-reacts with some diuretics/sulfonylureas), crystalluria, and photosensitivity.
Teach patients to increase fluid intake to prevent crystalluria and kidney stone formation.
Mechanism and uses of metronidazole
Answer: Disrupts DNA synthesis in anaerobic bacteria and protozoa; used for anaerobic infections, C. difficile, and trichomoniasis.
Signature adverse effect and teaching point for metronidazole
Answer: Disulfiram-like reaction with alcohol (flushing, nausea, vomiting); also causes a metallic taste.
Teach patients to avoid alcohol during treatment and for at least 48–72 hours after the last dose.
What does the RIPE acronym stand for in tuberculosis treatment?
Answer: Rifampin, Isoniazid, Pyrazinamide, Ethambutol — the first-line four-drug regimen for active TB.
Combination therapy is used to prevent resistance development.
Signature adverse effects of rifampin
Answer: Harmless orange-red discoloration of body fluids (urine, tears, sweat), hepatotoxicity, and strong induction of CYP450 enzymes (reduces efficacy of oral contraceptives and warfarin).
Teach patients that contact lenses may become permanently stained.
Signature adverse effect of isoniazid and how it's prevented
Answer: Peripheral neuropathy, prevented/treated by giving vitamin B6 (pyridoxine) supplementation; also causes hepatotoxicity.
Signature adverse effects of pyrazinamide
Answer: Hepatotoxicity and hyperuricemia (can trigger gout).
Signature adverse effect of ethambutol and required monitoring
Answer: Optic neuritis causing decreased visual acuity and red-green color blindness; requires baseline and periodic vision/color testing.
Teach patients to report any changes in vision immediately.
Monitoring required for all patients on TB therapy
Answer: Liver function tests (due to hepatotoxic potential of rifampin, isoniazid, and pyrazinamide) and assessment for medication adherence.
Directly observed therapy (DOT) is often used to ensure compliance given the long treatment duration (6+ months).
Compare mechanism and toxicity of amphotericin B vs. azole antifungals
Answer: Amphotericin B binds fungal cell membrane ergosterol causing cell leakage (nephrotoxic, causes infusion reactions "shake and bake"); azoles (e.g., fluconazole) inhibit ergosterol synthesis (hepatotoxic, many CYP450 drug interactions).
Premedicate for amphotericin B infusion reactions with antipyretics/antihistamines; monitor renal function closely.
Mechanism, use, and key adverse effect of acyclovir
Answer: Inhibits viral DNA polymerase to stop herpes virus replication; used for herpes simplex and varicella-zoster infections; main risk is nephrotoxicity (crystalluria).
Teach patients to maintain adequate hydration and that the drug does not cure the infection but reduces symptom severity/duration.
What are the main classes of antiretroviral (ART) drugs for HIV?
Answer: NRTIs (nucleoside reverse transcriptase inhibitors), NNRTIs (non-nucleoside RTIs), protease inhibitors, and integrase inhibitors — combined in multidrug regimens.
Combination therapy (HAART) reduces the risk of resistance developing.
Most important patient teaching point for antiretroviral therapy
Answer: Strict adherence to the exact dosing schedule is essential; missed doses promote drug resistance and treatment failure.
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