High-Yield Pharmacology Patterns: The USMLE Step 1 Guide
Pharmacology rewards pattern recognition more than memorizing isolated facts. A handful of patterns — what a drug-name stem means, which drugs speed or slow P-450 metabolism, how each toxidrome looks, and which antidote reverses which poison — answer a large share of board questions. This guide collects those patterns in one place, with short memory hooks, and links to the full guide for each drug class.
Evidence-based · For exam prep, not medical advice
update Updated October 2026
Date of last content change
Built by surgery and anesthesiology residents
Written for USMLE Step 1 · Free to read
bolt The 60-second version
Pharmacology rewards pattern recognition more than memorizing isolated facts. A handful of patterns — what a drug-name stem means, which drugs speed or slow P-450 metabolism, how each toxidrome looks, and which antidote reverses which poison — answer a large share of board questions.
check_circlePatterns are a starting point; confirm the mechanism behind each so you can reason through unfamiliar questions.
target What you'll be able to do · aligned to USMLE Step 1 · Pharmacology
PHARMIdentify drug classes from common generic-name stems.
PHARMRecall common cytochrome P-450 inducers and inhibitors and predict their interactions.
PHARMRecognize the major toxidromes and match poisons to their antidotes.
PHARMGroup drugs by the organ they damage to narrow toxicity questions.
How to use patterns for boards
Board questions rarely ask "what does drug X do?" Instead they describe a toxicity or a lab change and expect you to recognize the pattern. Learning patterns in groups — all P-450 inducers together, all pulmonary toxins together — makes recall faster than drug-by-drug lists.
workspace_premium Pattern first, mechanism second
Use a pattern to narrow the answer, then check it against the mechanism. A mnemonic without a mechanism breaks on a novel question; a mechanism without a pattern is slow.
Drug-name stems
Generic drug names follow naming conventions that encode the class.
Stem
Class
Example
-olol
β blocker
Metoprolol
-pril
ACE inhibitor
Lisinopril
-sartan
Angiotensin II receptor blocker
Losartan
-dipine
Dihydropyridine calcium channel blocker
Amlodipine
-statin
HMG-CoA reductase inhibitor
Atorvastatin
-xaban
Factor Xa inhibitor
Apixaban
-azole
Antifungal (ergosterol synthesis) or PPI (-prazole)
Fluconazole, omeprazole
-tidine
H2 receptor blocker
Famotidine
-floxacin
Fluoroquinolone
Ciprofloxacin
-cycline
Tetracycline
Doxycycline
-mab / -cept
Monoclonal antibody / receptor fusion protein
Infliximab / etanercept
-tinib
Tyrosine kinase inhibitor
Imatinib
-triptan
5-HT1B/1D agonist (migraine)
Sumatriptan
-osin
α1 blocker
Tamsulosin, prazosin
Monoclonal antibody names also encode the target and source: -ximab (chimeric), -zumab (humanized), -umab (human).
P-450 inducers and inhibitors
Most drug-interaction questions reduce to whether a new drug speeds up (induces) or slows down (inhibits) metabolism of an existing one.
P-450 interactions. Narrow-therapeutic-index drugs — warfarin, tacrolimus, cyclosporine, phenytoin, theophylline, and some statins — cause the most harm.
Toxidromes and antidotes
Recognizing a toxidrome identifies the drug class before any lab result.
Toxidromes. Skin moisture separates anticholinergic (dry) from sympathomimetic (sweaty) toxicity, which look otherwise similar.
Poison
Antidote
Acetaminophen
N-acetylcysteine
Opioids
Naloxone
Benzodiazepines
Flumazenil (rarely used — seizure risk)
Organophosphates
Atropine + pralidoxime
Anticholinergics
Physostigmine
TCAs
Sodium bicarbonate
β blockers
Glucagon
Digoxin
Digoxin immune Fab
Methanol, ethylene glycol
Fomepizole
Iron
Deferoxamine
Lead
Succimer, EDTA, dimercaprol
Cyanide
Hydroxocobalamin
Heparin
Protamine sulfate
Warfarin
Vitamin K + prothrombin complex concentrate
Methemoglobinemia
Methylene blue
Activated charcoal binds many ingested drugs but not alcohols, metals (iron, lithium), or caustics.
Toxicity by organ
Grouping drugs by the organ they damage turns a toxicity description into a short list of suspects.
Organ toxicity. Each guide linked below explains the mechanism behind these patterns.
functions Worked example — use two patterns together
A patient on long-term amiodarone for atrial fibrillation develops a dry cough and bilateral reticular opacities. The cardiologist also notes his warfarin requirement has dropped by half. Which two patterns explain the findings?
Pattern 1 — pulmonary fibrosis drugs: amiodarone is on the list.
1. A patient on oral contraceptives starts rifampin. What is the main risk?
Explanation. Rifampin induces CYP3A4, lowering estrogen and progestin levels.
2. A farmer has salivation, lacrimation, bronchorrhea, bradycardia, and pinpoint pupils. What is the treatment?
Explanation. Organophosphate poisoning causes a cholinergic toxidrome; atropine blocks muscarinic effects and pralidoxime regenerates acetylcholinesterase.
3. Which drug class is indicated by the stem "-xaban"?
Explanation. Apixaban, rivaroxaban, and edoxaban inhibit factor Xa.
Frequently asked questions
Which drugs induce cytochrome P-450?expand_more
Rifampin, carbamazepine, phenytoin, phenobarbital, griseofulvin, St John's wort, and chronic alcohol use. They lower levels of drugs metabolized by P-450.
Which drugs inhibit cytochrome P-450?expand_more
Azole antifungals, clarithromycin and erythromycin, protease inhibitors such as ritonavir, amiodarone, diltiazem, verapamil, cimetidine, and grapefruit juice.
How do you tell anticholinergic from sympathomimetic toxicity?expand_more
Both cause tachycardia, hyperthermia, and dilated pupils, but anticholinergic toxicity causes dry skin and urinary retention, while sympathomimetic toxicity causes sweating.
What is the antidote for acetaminophen overdose?expand_more
N-acetylcysteine, which replenishes glutathione to detoxify the toxic metabolite NAPQI. It is most effective within 8 hours of ingestion.
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