Antibiotics are drugs that either kill bacteria (bactericidal) or inhibit their growth (bacteriostatic), and they target structures or processes that are specific to bacteria, such as the cell wall, ribosomes, or DNA replication enzymes. Penicillins and cephalosporins are beta-lactam antibiotics that inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins and blocking cross-linking of peptidoglycan, ultimately leading to osmotic lysis of the bacterium. Cephalosporins are classified into generations, with first-generation agents such as cephalexin mainly active against gram-positive organisms, second-generation agents such as cefuroxime having broader coverage, third-generation agents such as ceftriaxone covering many gram-negative organisms, and fourth-generation agents such as cefepime providing broad coverage of both gram-positive and gram-negative bacteria. Macrolides such as erythromycin, azithromycin, and clarithromycin are bacteriostatic antibiotics that bind the 50S ribosomal subunit and inhibit bacterial protein synthesis, and they are commonly used for respiratory and skin infections and as alternatives in patients allergic to penicillin. Fluoroquinolones such as ciprofloxacin and levofloxacin are bactericidal drugs that inhibit DNA gyrase and topoisomerase IV, blocking DNA replication, and are used for urinary tract and respiratory infections, with notable adverse effects including tendon rupture and QT prolongation. Antibiotic resistance arises when bacteria evolve mechanisms such as beta-lactamase production, altered target sites, efflux pumps, and decreased permeability, and it is driven by overuse and misuse of these drugs. In immunocompromised patients, the distinction between bactericidal and bacteriostatic antibiotics becomes especially important, because bactericidal agents are often preferred when host defenses are impaired.
Antifungal drugs similarly target structures specific to fungi. Azoles such as fluconazole inhibit the synthesis of ergosterol, a key component of the fungal cell membrane; polyenes such as amphotericin B bind directly to ergosterol and disrupt the membrane; echinocandins such as caspofungin inhibit the synthesis of cell wall glucan; and allylamines such as terbinafine inhibit squalene epoxidase, also in ergosterol synthesis. Antiviral drugs target specific steps in viral replication, including acyclovir, which inhibits viral DNA polymerase in herpesvirus infections, oseltamivir, a neuraminidase inhibitor used in influenza, and the multiple classes of antiretrovirals used in HIV, although vaccines remain the preferred strategy for prevention.
Analgesics relieve pain through several distinct mechanisms. Non-opioid analgesics include the nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. NSAIDs such as ibuprofen, naproxen, and aspirin inhibit cyclooxygenase enzymes, reducing the production of prostaglandins that mediate pain, inflammation, and fever. COX-1 is a constitutive enzyme that protects the stomach lining, supports kidney function, and promotes platelet aggregation, while COX-2 is induced at sites of inflammation and pain; non-selective NSAIDs inhibit both, whereas selective COX-2 inhibitors such as celecoxib spare COX-1. Aspirin is unique in that it irreversibly acetylates COX-1 and COX-2; at low doses of about 81 mg, this produces an antiplatelet effect by preventing thromboxane A2 synthesis, while higher doses are required for analgesic and anti-inflammatory action. Acetaminophen is believed to act primarily in the central nervous system by inhibiting COX enzymes, producing analgesia and antipyresis with little peripheral anti-inflammatory effect and minimal gastrointestinal irritation, although hepatotoxicity becomes a serious concern at doses above about 4 g per day. Opioids such as morphine, codeine, and oxycodone bind to mu, delta, and kappa opioid receptors, particularly mu receptors, which mediate analgesia as well as respiratory depression, sedation, and the most common side effect, constipation. Naloxone is a competitive opioid antagonist used to rapidly reverse opioid overdose, given intravenously, intramuscularly, or intranasally, with the caveat that its duration of action is shorter than that of most opioids, so redosing may be required.