Common Drug Classes

Why This Matters

In pharmacology, you're not just memorizing drug names—you're learning to think in terms of mechanisms of action, therapeutic goals, and monitoring parameters. Every drug class on this list represents a different strategy for intervening in the body's physiology, whether that's blocking a receptor, inhibiting an enzyme, or altering ion movement across cell membranes. Understanding why a drug works helps you predict its effects, side effects, and interactions.

The exam will test your ability to connect drug classes to their mechanisms, identify appropriate monitoring parameters, and recognize when one drug might be preferred over another. Don't just memorize that "beta-blockers treat hypertension"—know that they work by reducing cardiac output and renin release, which is why they're also useful for heart failure and anxiety. That kind of conceptual thinking is what separates strong exam performance from rote memorization.

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Drugs That Modulate Pain and Inflammation

Pain management represents one of the most fundamental applications of pharmacology. These drugs work through different mechanisms—blocking prostaglandin synthesis, activating opioid receptors, or both—and understanding these pathways helps you predict both therapeutic effects and adverse reactions.

Analgesics

• Two major categories: opioid and non-opioid—opioids (morphine, oxycodone) bind to mu receptors in the CNS, while non-opioids (acetaminophen) work primarily through central mechanisms without anti-inflammatory effects
• Opioid dependence and respiratory depression are the critical safety concerns, requiring careful dose titration and monitoring of respiratory rate and sedation level
• Non-opioids are first-line for mild-moderate pain—they avoid the dependence risk and are often combined with opioids for synergistic effects in moderate-severe pain

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

• Inhibit cyclooxygenase (COX) enzymes—blocking prostaglandin synthesis provides the triple effect of analgesia, anti-inflammatory action, and antipyretic activity
• GI bleeding and renal impairment are the major adverse effects, since prostaglandins normally protect gastric mucosa and maintain renal blood flow
• Common examples include ibuprofen and naproxen—COX-2 selective inhibitors (celecoxib) reduce GI risk but carry cardiovascular concerns

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Drugs That Target the Cardiovascular System

Cardiovascular pharmacology centers on four key goals: controlling blood pressure, preventing clots, managing heart rhythm, and reducing atherosclerosis. These drugs often work together, and understanding their mechanisms helps you anticipate both therapeutic synergy and dangerous interactions.

Antihypertensives

• Multiple drug classes with distinct mechanisms—diuretics reduce volume, ACE inhibitors block the renin-angiotensin system, beta-blockers decrease cardiac output, and calcium channel blockers cause vasodilation
• Blood pressure monitoring is essential for assessing effectiveness and guiding dose adjustments; target values vary based on patient comorbidities
• First-line choices depend on patient factors—ACE inhibitors are preferred in diabetes (renal protection), beta-blockers in heart failure, thiazides in uncomplicated hypertension

Anticoagulants

• Prevent clot formation through different pathways—warfarin inhibits vitamin K-dependent clotting factors, while DOACs (rivaroxaban, apixaban) directly inhibit factor Xa or thrombin
• Warfarin requires INR monitoring (target typically 2-3) due to narrow therapeutic index and numerous drug-food interactions
• DOACs offer predictable dosing without routine monitoring—but lack reliable reversal agents for some, and renal function affects dosing

Statins

• Inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, reducing LDL levels by 30-50% depending on dose and agent
• Atorvastatin and simvastatin are common examples; high-intensity therapy is standard for secondary prevention after cardiovascular events
• Monitor liver enzymes and muscle symptoms—myopathy and rhabdomyolysis are rare but serious adverse effects requiring immediate attention

Diuretics

• Promote sodium and water excretion at different nephron sites—loop diuretics (furosemide) at the ascending loop, thiazides at the distal tubule, potassium-sparing (spironolactone) at the collecting duct
• Electrolyte monitoring is critical—loop and thiazide diuretics cause hypokalemia, while potassium-sparing diuretics risk hyperkalemia
• Used for hypertension, heart failure, and edema—loop diuretics are most potent for acute fluid removal, thiazides preferred for chronic hypertension management

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Drugs That Regulate Metabolism and Endocrine Function

Metabolic disorders require drugs that either replace deficient hormones or modify cellular responses to existing hormones. Blood glucose management exemplifies how pharmacology must balance efficacy against hypoglycemia risk.

Antidiabetics

• Insulin is essential for Type 1 and often needed in Type 2—it directly facilitates glucose uptake into cells; available in rapid, short, intermediate, and long-acting formulations
• Metformin is first-line for Type 2 diabetes—it decreases hepatic glucose production and improves insulin sensitivity without causing hypoglycemia
• Blood glucose monitoring guides therapy adjustments—target HbA1c typically <7%, though individualized based on patient factors and hypoglycemia risk

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Drugs That Fight Infection

Anti-infective pharmacology requires understanding not just what kills pathogens, but how resistance develops and why appropriate use matters for public health. The mechanism of action determines which organisms are susceptible.

Antibiotics

• Work by killing bacteria (bactericidal) or inhibiting growth (bacteriostatic)—mechanisms include cell wall synthesis inhibition (penicillins, cephalosporins), protein synthesis inhibition (macrolides), and DNA replication interference (fluoroquinolones)
• Completing the full course prevents resistance—subtherapeutic exposure allows resistant organisms to survive and proliferate
• Spectrum of activity varies by class—narrow-spectrum agents target specific bacteria, while broad-spectrum agents (useful empirically) increase resistance risk

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Drugs That Modulate the Central Nervous System

CNS pharmacology involves drugs that alter neurotransmitter activity—increasing, decreasing, or modulating signals at synapses. These drugs often have delayed onset of therapeutic effect and require careful monitoring for both efficacy and adverse effects.

Antidepressants

• SSRIs (fluoxetine, sertraline) are first-line for depression and anxiety—they selectively block serotonin reuptake, increasing synaptic serotonin availability
• Therapeutic effects take 2-4 weeks to develop—patients need education about this delay and close monitoring for worsening symptoms, especially early in treatment
• Other classes include SNRIs and tricyclics—SNRIs add norepinephrine reuptake inhibition; tricyclics are effective but have more side effects and overdose risk

Antipsychotics

• Block dopamine D2 receptors to reduce positive symptoms of psychosis (hallucinations, delusions); atypical agents also affect serotonin receptors
• First-generation (typical) vs. second-generation (atypical)—typicals (haloperidol) have higher risk of movement disorders; atypicals (risperidone, olanzapine) have higher metabolic risk
• Monitor for extrapyramidal symptoms and metabolic syndrome—weight gain, glucose intolerance, and lipid abnormalities require regular screening with atypical agents

Antiepileptics

• Stabilize neuronal membranes through various mechanisms—sodium channel blockade (phenytoin, carbamazepine), GABA enhancement (valproate, benzodiazepines), or calcium channel effects (ethosuximide)
• Drug level monitoring is essential for many agents due to narrow therapeutic indices and significant drug interactions
• Choice depends on seizure type—phenytoin and carbamazepine for focal seizures, valproate and lamotrigine for generalized seizures, ethosuximide specifically for absence seizures

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Drugs That Affect the Respiratory and GI Systems

These drug classes address common conditions through receptor blockade or enzyme inhibition. Understanding the underlying physiology of allergic responses, bronchoconstriction, and acid secretion clarifies why these drugs work.

Antihistamines

• Block H1 histamine receptors to prevent allergic symptoms—histamine release from mast cells causes vasodilation, increased permeability, and itching
• First-generation (diphenhydramine) crosses the blood-brain barrier—causing sedation, which can be therapeutic (sleep aids) or problematic (impaired function)
• Second-generation (loratadine, cetirizine) are non-sedating—preferred for daytime allergy management due to reduced CNS penetration

Bronchodilators

• Relax bronchial smooth muscle through beta-2 receptor activation (sympathomimetics) or muscarinic receptor blockade (anticholinergics)
• Short-acting agents (albuterol) for acute relief—onset within minutes, used as rescue medication for asthma attacks
• Long-acting agents (salmeterol, tiotropium) for maintenance—never used alone for asthma; always combined with inhaled corticosteroids

Proton Pump Inhibitors

• Irreversibly inhibit the gastric H+/K+ ATPase—the final step in acid secretion, providing more complete acid suppression than H2 blockers
• Omeprazole and esomeprazole are common examples; most effective when taken 30-60 minutes before meals
• Long-term use concerns include vitamin B12 and magnesium deficiency, increased infection risk (C. difficile), and possible bone fracture risk

Antiemetics

• Target different receptors depending on nausea etiology—serotonin antagonists (ondansetron) for chemotherapy-induced nausea, dopamine antagonists (metoclopramide) for gastroparesis, anticholinergics for motion sickness
• Ondansetron is first-line for chemotherapy and post-operative nausea—blocks 5-HT3 receptors in the chemoreceptor trigger zone
• Identifying the underlying cause guides drug selection—vestibular causes respond to anticholinergics, while delayed gastric emptying responds to prokinetic agents

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Quick Reference Table

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Self-Check Questions

1. Which two drug classes both reduce cardiovascular risk but through completely different mechanisms—one by lowering cholesterol synthesis and one by preventing clot formation?

2. A patient on warfarin asks why they need regular blood tests while their neighbor on apixaban doesn't. How would you explain the difference in monitoring requirements based on their mechanisms?

3. Compare first-generation and second-generation antihistamines: what property makes second-generation agents preferred for daytime use, and what is the pharmacokinetic reason for this difference?

4. If a patient with Type 2 diabetes is started on metformin, why is hypoglycemia less of a concern compared to a patient started on insulin? What mechanism explains this difference?

5. An exam question describes a patient with asthma using their albuterol inhaler multiple times daily. What does this pattern indicate about their disease control, and what class of medication should be added to their regimen?