Pharmacology Mnemonics for USMLE Step 1: Drug Classes, Mechanisms, and Side Effects

A ValueMD community study resource, originally shared on our forums and preserved here for students working through pharmacology for Step 1.

Pharmacology is arguably the single most mnemonic-dependent subject on Step 1: hundreds of drugs, each with its own mechanism, indication, and side-effect profile, that all start to blur together without memory hooks. This is one of the largest and most detailed mnemonic collections built by the ValueMD community, covering cardiovascular, CNS, antimicrobial, endocrine, and oncologic pharmacology, along with a condensed mechanism-of-action reference.

Educational note: these are student-built memory aids for exam review, not a substitute for a pharmacology textbook, First Aid, or your course material. A number of entries below have been corrected, consolidated, or updated from the original forum thread, several contained real factual errors rather than just stylistic issues, and a few reflect prescribing patterns that have since changed. Details are noted inline.

Cardiovascular Pharmacology

Beta Blockers: Cardioselective (B1) vs. Non-Selective

Cardioselective (B1-selective): Acebutolol, Atenolol, Esmolol, Metoprolol, remembered as BEAM ONE up, Scotty (Bisoprolol is also commonly grouped here).

Non-selective (B1 and B2): Nadolol, Pindolol, Propranolol, Timolol, Sotalol.

Beta Blockers with Intrinsic Sympathomimetic Activity (ISA)

Pindolol and acebutolol have partial agonist activity, making them relatively more acceptable in some patients with asthma or diabetes, despite being non-selective or having beta-blocking effects, since they don’t fully block sympathetic tone.

Beta Blockers Requiring Dose Adjustment for CYP2D6 Polymorphism

“I Met Tim Carver, the metabolic polymorph”: Metoprolol, Timolol, and Carvedilol require dose adjustment in patients with higher or lower than normal CYP2D6 activity.

Beta Blockers: Side Effects

“BBC Loses Viewers In Rochedale”: Bradycardia, Bronchoconstriction, Claudication, dyslipidemia (Lipids), Vivid dreams and nightmares, negative Inotropic action, and Reduced awareness of hypoglycemia.

Alpha vs. Beta Adrenoceptors: Vasomotor Effect

A simplified rule: alpha receptors generally constrict, beta receptors (specifically beta-2) generally dilate. (Beta-1 is primarily cardiac and doesn’t have a vasomotor role; this rule of thumb applies to vascular smooth muscle.)

Beta-1 vs. Beta-2 Receptor Location

“You have 1 heart and 2 lungs”: beta-1 receptors are primarily on the heart; beta-2 receptors are primarily in the lungs (and vasculature).

Calcium Channel Blockers: Clinical Uses

CHASM: Cerebral vasospasm, Hypertension, Angina, Supraventricular tachyarrhythmia, Migraine prophylaxis. (Note: routine use in heart failure is more nuanced than this mnemonic implies, non-dihydropyridine CCBs like verapamil and diltiazem are generally avoided in reduced-ejection-fraction heart failure, while dihydropyridines like amlodipine are sometimes used cautiously.)

Antiarrhythmic Classification (Vaughan-Williams)

“MBA College”, Class I to IV in order: Membrane stabilizers (Class I), Beta blockers (Class II), Action-potential-widening agents (Class III), Calcium channel blockers (Class IV).

Antiarrhythmics: Class III Members

BIAS: Bretylium, Ibutilide, Amiodarone, Sotalol.

Amiodarone: Action and Side Effects (6 P’s)

Prolongs action potential duration, Photosensitivity, Pigmentation of the skin, Peripheral neuropathy, Pulmonary alveolitis and fibrosis, and Peripheral conversion of T4 to T3 is inhibited, leading to hypothyroidism.

Drugs That Prolong QT and Can Cause Torsades de Pointes

APACHE: Amiodarone, Procainamide, Arsenic trioxide, Cisapride, Haloperidol, Erythromycin (the original phrasing miswrote “Arsenium” and “Eritromycin”).

Warfarin: Mechanism and Monitoring

WEPT: Warfarin works on the Extrinsic pathway and is monitored by PT.

Additional properties, SLOW: Small lipid-soluble molecule, Liver is the site of action, Oral route of administration, Warfarin has a slow onset despite quickly antagonizing vitamin K.

Enoxaparin (a Low Molecular Weight Heparin)

Enoxaparin acts specifically on factor Xa, so it’s monitored using anti-Xa levels rather than aPTT.

Thrombolytic Agents

USA: Urokinase, Streptokinase, Alteplase (tPA). (Newer agents like tenecteplase and reteplase are also now widely used.)

Hypertension Treatment Classes

ABCD: ACE inhibitors/Angiotensin II antagonists (sometimes alpha agonists), Beta blockers, Calcium channel blockers, Diuretics.

Thiazide Diuretics: Indications

“CHIC to use thiazides”: CHF, Hypertension, [nephrogenic diabetes] Insipidus, Calcium calculi (thiazides reduce urinary calcium excretion).

Osmotic Diuretics

GUM: Glycerol, Urea, Mannitol.

Migraine Prophylaxis Drugs

“Very Volatile Pharmacotherapeutic Agents For Migraine Prophylaxis”: Verapamil, Valproic acid, Pizotifen, Amitriptyline, Flunarizine, Methysergide, Propranolol.

CNS and Psychiatric Pharmacology

MPTP: Mechanism

MPTP is a Mitochondrial Parkinson’s-Type Poison, a mitochondrial toxin (inhibiting Complex I) that produces a Parkinson’s-like syndrome.

Tricyclic Antidepressants Worth Knowing

“I have to hide, the CIA is after me”: Clomipramine, Imipramine, Amitriptyline. A second tier, “the DND is also after me”: Desipramine, Nortriptyline, Doxepin.

MAOIs: Members and Indications

Members, “PIT of despair”: Phenelzine, Isocarboxazid, Tranylcypromine.

Indications, MAOI’S: Melancholic (atypical depression), Anxiety disorders, Obesity-spectrum disorders (bulimia), Imagined illnesses (hypochondriasis), Social phobia. Note that MAOIs are rarely first-line today given their dietary restrictions and drug interaction risks; they’re generally reserved for treatment-resistant cases.

SSRIs: Side Effects

SSRI: Serotonin syndrome risk, Stimulation of the CNS (insomnia, anxiety), Reproductive/sexual dysfunction (in both men and women), Insomnia.

Serotonin Syndrome: Core Features

HARM: Hyperthermia, Autonomic instability, Rigidity, Myoclonus.

Drugs That Can Induce Depression

PROMS: Propranolol, Reserpine, Oral contraceptives, Methyldopa, Steroids.

Benzodiazepines Safe in Liver Failure

LOT: Lorazepam, Oxazepam, Temazepam, metabolized by glucuronidation rather than oxidation, so they’re preferred in hepatic impairment.

Benzodiazepines: Core Actions

Sedation, anti-Convulsant activity, anti-Anxiety effect, and muscle relaxation, notably without any antipsychotic activity.

Benzodiazepines: Drugs That Slow Their Metabolism

“I’m Overly Calm”: Isoniazid, Oral contraceptives, Cimetidine, all inhibit hepatic metabolism, increasing benzodiazepine effect.

Benzodiazepine Antidote

Flumazenil reverses benzodiazepine effects.

Anesthesia: The Four Classic Stages

“Anesthesiologists Enjoy S & M”: Analgesia, Excitement, Surgical anesthesia, Medullary paralysis.

Inhalational Anesthetics

SHINE: Sevoflurane, Halothane, Isoflurane, Nitrous oxide, Enflurane. Add the now-defunct Methoxyflurane and it becomes “MoonSHINE.”

4-Aminopyridine (4-AP)

Used for AP (action potential) propagation in multiple sclerosis (marketed as dalfampridine).

Autonomic Pharmacology

Muscarinic Effects (Cholinergic Toxicity)

SLUG BAM: Salivation/Secretions/Sweating, Lacrimation, Urination, GI upset, Bradycardia/Bronchoconstriction/Bowel activity, Abdominal cramps/Anorexia, Miosis.

A closely related version for organophosphate poisoning, “LESS DUMB”: Lacrimation, Excitation of nicotinic synapses, Salivation, Sweating, Diarrhea, Urination, Micturition, Bronchoconstriction.

Antimuscarinic Drugs

“Inhibits Parasympathetic And Sweat”: Ipratropium, Pirenzepine, Atropine, Scopolamine, all act at muscarinic receptors found at parasympathetic nerve endings and at sweat glands (which are sympathetically innervated but cholinergic).

Anticholinergic Side Effects

ABCD’S: Anorexia, Blurry vision, Constipation/Confusion, Dry mouth, Sedation/Stasis of urine (urinary retention).

Atropine: Use in Bradycardia

“A goes with B”: Atropine is used to treat Bradycardia.

Ipratropium: Mechanism

Atropine is hidden in the middle of the word: iprAtropium, so it behaves like atropine (an antimuscarinic).

Direct-Acting Sympathomimetic Catecholamines

DINED: Dopamine, Isoproterenol, Norepinephrine, Epinephrine, Dobutamine.

Reserpine: Mechanism

Reserpine depletes the reserves of catecholamines and serotonin (by blocking vesicular monoamine transport).

Toxicology and Overdose

Therapeutic vs. Toxic Drug Levels: “The Magic 2’s”

Approximate reference values, always confirm against current lab and clinical guidelines rather than relying on a mnemonic alone:

Zero-Order Kinetics Drugs

PEAZ: Phenytoin, Ethanol, Aspirin (at high/toxic doses), all follow Zero-order kinetics, meaning a constant amount is eliminated per unit time regardless of concentration.

Drugs Causing Focal to Massive Hepatic Necrosis

“Very Angry Hepatocytes”: Valproic acid, Acetaminophen, Halothane (isoniazid and Amanita mushroom toxin are other important causes).

Respiratory Depression: Drug Categories to Watch

Sedative-hypnotics, opioids, and agents that impair neuromuscular transmission (such as aminoglycosides and polymyxins) can all contribute to respiratory depression, particularly in combination or in vulnerable patients.

Delirium-Inducing Drugs in Elderly Patients

“ACUTE CHANGE IN MS”: Antibiotics, Cardiac drugs (digoxin, lidocaine), Urinary incontinence drugs (anticholinergics), Theophylline, Ethanol, Corticosteroids, H2 blockers, Antiparkinsonian drugs, Narcotics (especially meperidine), Geriatric psychiatric drugs, ENT drugs, Insomnia drugs, NSAIDs, Muscle relaxants, Seizure medications.

Disulfiram-Like Reaction Drugs

“PM PMT”: Procarbazine, Metronidazole, and certain cephalosporins with an MTT side chain (cefoperazone, cefamandole, cefotetan).

Routes of Drug/Toxin Entry: Fastest to Slowest

“Stick it, Sniff it, Suck it, Soak it”: injection (Stick), inhalation (Sniff), ingestion (Suck), and absorption through skin (Soak).

Endocrine and Reproductive Pharmacology

Steroid Side Effects (CUSHINGOID)

Cataracts, Ulcers, Skin changes (striae, thinning, bruising), Hypertension/Hirsutism/Hyperglycemia, Infections, avascular Necrosis of the femoral head, Glycosuria, Osteoporosis/Obesity, Immunosuppression, Diabetes. This covers the same territory as a longer alternate version some students use built around the word “BECLOMETHASONE.”

Propylthiouracil (PTU): Mechanism

Inhibits Peroxidase, Peripheral deiodination of T4 to T3, and Tyrosine iodination/coupling (Union).

Methyldopa: Side Effects

METHYLDOPA: Mental effects (sedation), Electrolyte imbalance/Edema, Tolerance, Headache/Hepatotoxicity/psychological upset, Lactation (galactorrhea), Dry mouth, Edema, Parkinsonism-like symptoms, Anemia (hemolytic, Coombs-positive).

Lithium: Side Effects

LITH: Leukocytosis, [diabetes] Insipidus (nephrogenic), Tremor/Teratogenesis (associated with Ebstein anomaly), Hypothyroidism.

Sodium Valproate: Side Effects

VALPROATE: Vomiting, Alopecia, Liver toxicity, Pancreatitis/Pancytopenia, Retention of fluid (weight gain), Edema, Appetite increase, Tremor, Enzyme induction (hepatic).

Phenytoin: Adverse Effects

PHENYTOIN: P-450 interactions, Hirsutism, Enlarged gums (gingival hyperplasia), Nystagmus, Yellow-browning of skin, Teratogenicity, Osteomalacia, Interference with folate metabolism (leading to megaloblastic anemia, the original mnemonic mislabeled this as B12), Neuropathies including vertigo and ataxia.

Gynecomastia-Causing Drugs

DISCOS: Digoxin, Isoniazid, Spironolactone, Cimetidine, Oestrogens, Stilbestrol (ketoconazole and marijuana are other commonly cited causes).

SIADH-Inducing Drugs

ABCD: Analgesics (opioids, NSAIDs), Barbiturates, Cyclophosphamide/Chlorpromazine/Carbamazepine, Diuretics (thiazides). SSRIs are another very commonly cited cause not captured in this older mnemonic.

Teratogenic Drugs

A shorter list, TAP CAP: Thalidomide, Androgens, Progestins, Corticosteroids, Aspirin and indomethacin, Phenytoin.

A more complete version, “W/ TERATOgenic”: Warfarin, Thalidomide, Epileptic drugs (phenytoin, valproate, carbamazepine), Retinoids, ACE inhibitors, Third element (lithium), OCPs and other hormones (such as danazol).

K+-Increasing Agents

K-BANK: K-sparing diuretics, Beta blockers, ACE inhibitors, NSAIDs, K supplements.

Antimicrobial and Antiviral Pharmacology

Quinolones and Fluoroquinolones: Mechanism

“Topple the Queen”: quinolones interfere with topoisomerase II (DNA gyrase) and topoisomerase IV.

Sulfonamides: Major Side Effects

Stevens-Johnson syndrome, skin rash, low solubility (causing crystalluria), and displacement of drugs bound to serum albumin (causing neonatal kernicterus and potentiating other albumin-bound drugs like warfarin).

TB First-Line Antibiotics

STRIPE: Streptomycin, Rifampin, Isoniazid, Pyrazinamide, Ethambutol.

Antibiotics Generally Avoided in Pregnancy

MCAT: Metronidazole (particularly avoided in the first trimester), Chloramphenicol (gray baby syndrome), Aminoglycosides (fetal ototoxicity), Tetracyclines (fetal teeth and bone effects). Fluoroquinolones are also generally avoided due to potential cartilage effects.

Ribavirin: Indications

Ribavirin is used for RSV (particularly inhaled, in select infants) and for viral hemorrhagic fevers caused by arenaviruses (such as Lassa fever); it has also historically been combined with interferon for hepatitis C, though this has largely been replaced by direct-acting antivirals.

“-vir” Named Drugs

A drug name containing “-vir,” whether at the start, middle, or end, generally signals an antiviral: Abacavir, Acyclovir, Amprenavir, Cidofovir, Efavirenz, Indinavir, Ganciclovir, Oseltamivir, Ritonavir, Saquinavir, Valacyclovir, Zanamivir.

Asthma Leukotriene-Pathway Drugs

Zafirlukast and Montelukast are leukotriene receptor antagonists; Zileuton inhibits 5-lipoxygenase (5-LO), the enzyme that produces leukotrienes.

Oncology and Chemotherapy

Drugs Causing Pulmonary Fibrosis/Infiltrates

“Go BAN Me”: Gold, Bleomycin, Busulfan, BCNU (carmustine), Amiodarone, Nitrofurantoin, Methotrexate, Methysergide.

Busulfan: Key Features

ABCDEF: Alkylating agent, Bone marrow suppression, CML is the classic indication, Dark skin (hyperpigmentation), Endocrine insufficiency (adrenal, a “pseudo-Addison” picture), Fibrosis (pulmonary).

Cisplatin: Mechanism and Major Toxicity

Cisplatin forms DNA cross-links, interfering with replication and transcription. It’s highly emetogenic (severe nausea and vomiting is characteristic), and its major dose-limiting toxicities are nephrotoxicity and ototoxicity.

Bleomycin: Mechanism

Bleomycin generates free radicals that fragment DNA strands; its major dose-limiting toxicity is pulmonary fibrosis.

Chemotherapy Agents Affecting DNA and Transcription

A broad grouping of agents that interfere with DNA integrity or gene expression: Alkylating agents, Bleomycin, Cisplatin, Dactinomycin and Doxorubicin, Etoposide, and hormone-pathway agents like Flutamide and Tamoxifen.

Opioid Pharmacology

Opioid Mu-Receptor Effects

MD CARES: Miosis, Dependency, Constipation, Analgesia, Respiratory depression, Euphoria, Sedation. A shorter version, PEAR: Physical dependence, Euphoria, Analgesia, Respiratory depression.

Opioid Effects, More Broadly

“BAD AMERICANS”: Bradycardia and hypotension, Anorexia, Diminished pupillary size, Analgesia, Miosis, Euphoria, Respiratory depression, Increased smooth muscle activity (biliary tract constriction), Constipation, Ameliorated cough reflex, Nausea and vomiting, Sedation.

Narcotics: Side Effects

“SCRAM if you see a drug dealer”: Synergistic CNS depression with other drugs, Constipation, Respiratory depression, Addiction, Miosis.

Narcotic Antagonists

Naloxone and Naltrexone, used clinically to treat narcotic overdose.

Other High-Yield Drug Facts

Physostigmine vs. Neostigmine

LMNOP describes physostigmine: Lipid-soluble, Miotic, Natural, Orally absorbed well, Physostigmine (crosses the blood-brain barrier, used for anticholinergic toxicity). Neostigmine, by contrast, is water-soluble, synthetic, poorly absorbed orally, and used in myasthenia gravis (doesn’t cross the blood-brain barrier).

Myasthenia Gravis: Edrophonium vs. Pyridostigmine

Edrophonium is used for Diagnosis (short-acting); pyridostigmine is used to get RID of ongoing symptoms (long-acting treatment).

Succinylcholine: Action

Succinylcholine binds the acetylcholine receptor and keeps it open, producing sustained depolarization before blockade; it’s used clinically for rapid-sequence intubation.

Botulinum Toxin: Mechanism

Botulinum toxin blocks the release of acetylcholine at the neuromuscular junction. It acts presynaptically, similar to beta-bungarotoxin (alpha-bungarotoxin, by contrast, acts postsynaptically by blocking nicotinic receptors).

Prazosin: Use

An alpha-1 blocker used for hypertension and for urinary retention symptoms associated with BPH.

Phenobarbital: Age-Dependent Side Effects

Children tend to become more agitated (hyperkinesia, irritability, insomnia, aggression); adults tend to become sedated (drowsiness, dizziness).

Tetracycline: Teratogenicity

Tetracycline is a teratogen that causes staining of teeth in children exposed in utero or during early childhood.

Patent Ductus Arteriosus: Pharmacologic Closure

“Come In and Close the door”: Indomethacin (or ibuprofen) is used to pharmacologically close a PDA.

Lead Poisoning: Presentation

ABCDEFG: Anemia, Basophilic stippling, Colicky abdominal pain, Constipation (not diarrhea, the classic GI presentation of lead poisoning is constipation and colicky pain), Encephalopathy, Foot/wrist drop (peripheral neuropathy), Gum lines (Burton’s line).

Fundamentals of Pharmacodynamics

• Agonists bind receptors and stimulate them; antagonists bind receptors and block or reduce an agonist’s effect without stimulating the receptor themselves.
• A competitive antagonist binds reversibly and can be overcome by more agonist; a non-competitive antagonist typically binds irreversibly (or at a different site) and can’t be overcome by adding more agonist.
• Efficacy is the maximal effect a drug can produce. Potency is how much drug is needed to produce a given effect, driven by receptor affinity and the drug’s ability to reach its target.
• ED50 is the dose producing a half-maximal response in the population (a measure of potency, lower ED50 means more potent). TD50 is the dose producing a defined toxic effect in half the population. LD50 is the dose lethal to half the population (in animal studies).
• Therapeutic index is the ratio of the toxic (or lethal) dose to the effective dose: TI = TD50 / ED50 (or LD50 / ED50). A higher therapeutic index generally means a safer drug.
• Pharmacogenetics example: isoniazid is metabolized by hepatic acetylation, and the speed of acetylation (fast vs. slow acetylator) is genetically determined and affects both efficacy and toxicity risk.

Selected Drug Mechanisms, Uses, and Toxicities

A condensed reference covering several commonly tested individual agents:

• Scopolamine: antimuscarinic, used for motion sickness and preoperatively to reduce secretions; toxicity produces classic antimuscarinic effects (mydriasis, cycloplegia, decreased secretions, flushing, urinary retention, drowsiness, and at high doses, hallucinations).
• Typical antipsychotics (chlorpromazine, haloperidol, thioridazine): dopamine antagonists used for schizophrenia and psychosis; cause extrapyramidal effects (parkinsonism, akathisia, tardive dyskinesia) and anticholinergic/antihistamine effects. Higher potency (haloperidol > chlorpromazine > thioridazine) generally correlates with more extrapyramidal effects and fewer anticholinergic effects.
• Atypical antipsychotics (e.g., clozapine): fewer extrapyramidal effects, but clozapine carries a risk of agranulocytosis and neuroleptic malignant syndrome.
• Opioid agonists (morphine, meperidine, codeine, methadone, fentanyl): act at mu, kappa, and delta receptors for analgesia; codeine is also used as an antitussive, methadone for opioid use disorder treatment, and loperamide as an antidiarrheal.
• Opioid antagonists (naloxone, naltrexone): block opioid receptors, used for overdose reversal.
• Erythropoietin: increases red blood cell production, used for anemia associated with renal failure or chemotherapy.
• Mifepristone (RU-486): a progesterone receptor antagonist used for early-term medical abortion.
• Acarbose: alpha-glucosidase inhibitor that decreases glucose absorption, used in type 2 diabetes; common side effects include flatulence and GI upset.
• Losartan: an angiotensin II receptor antagonist; similar antihypertensive effect to ACE inhibitors but without the cough, since it doesn’t affect bradykinin metabolism.
• Cholinesterase inhibitors (edrophonium, neostigmine, pyridostigmine): used in myasthenia gravis diagnosis and treatment, open-angle glaucoma, and to reverse non-depolarizing neuromuscular blockade; can cause fasciculations and muscle weakness.
• Leuprolide: a GnRH analog that, with continuous use, desensitizes pituitary receptors and lowers LH/FSH; used in prostate cancer, typically combined with flutamide to prevent an initial testosterone flare.
• Aminoglutethimide: inhibits the conversion of cholesterol to pregnenolone; historically used in metastatic breast cancer, though largely superseded today by aromatase inhibitors.
• Metformin: decreases hepatic gluconeogenesis and improves lipid profile; first-line for type 2 diabetes, with a low hypoglycemia risk, but carries rare risk of lactic acidosis and long-term interference with B12 absorption.

Additional Clinical Pearls

Corticosteroids

Synthesized in the adrenal cortex; catabolic effects on carbohydrate and fat metabolism; decrease intestinal calcium uptake while increasing renal calcium excretion (contributing to osteoporosis); suppress inflammation by inhibiting phospholipase A2 (reducing prostaglandin and leukotriene production). Common agents include cortisone, prednisone, prednisolone, methylprednisolone, triamcinolone, dexamethasone, and beclomethasone. Toxicity includes hirsutism, skin thinning, poor wound healing, striae, hyperglycemia, hypertension, cataracts, glaucoma, peptic ulcer disease, osteoporosis, and increased infection risk.

Antifungals (Brief Overview)

Polyene antibiotics (amphotericin B, nystatin) bind fungal membrane ergosterol, causing leakage and cell death; amphotericin B is used for systemic infections (with fever, chills, renal impairment, and anemia as key toxicities), while nystatin is mainly topical. Imidazoles (miconazole, clotrimazole, ketoconazole) block fungal ergosterol synthesis. Flucytosine is often combined with amphotericin B for cryptococcal meningitis. Griseofulvin binds keratin and treats dermatophyte (tinea) infections.

Treatment of Anemia

Microcytic anemia often responds to oral or IV iron. Megaloblastic anemia can result from B12 deficiency (which also causes neurologic symptoms and requires intrinsic factor for absorption) or folate deficiency (which does not cause neurologic symptoms and is well absorbed orally); folate replacement will correct the anemia but not any neurologic deficits from B12 deficiency. Erythropoietin and colony-stimulating factors (G-CSF, GM-CSF) support red and white cell production respectively in the setting of renal failure or myelosuppressive chemotherapy.

Stroke Prevention

Aspirin irreversibly blocks cyclooxygenase, reducing thromboxane A2-mediated platelet aggregation, at a low daily dose. Ticlopidine inhibits platelet aggregation via the ADP pathway, though it has been largely replaced in modern practice by clopidogrel due to ticlopidine’s risk of blood dyscrasias. Thrombolytics (streptokinase, urokinase, tPA) promote a generalized lytic state by catalyzing plasmin formation.

Rheumatoid Arthritis Treatment (Classic Framework)

Pain management historically centered on aspirin, NSAIDs, and COX-2 inhibitors, while disease-modifying agents included methotrexate, immunosuppressives, and gold compounds (with dermatitis as a common gold side effect). Note that modern rheumatoid arthritis treatment now centers heavily on biologic DMARDs (such as TNF inhibitors), which weren’t part of this older mnemonic framework.

Antirheumatic (Disease-Modifying) Agents

CHAMP: Cyclophosphamide, Hydroxychloroquine/chloroquine, Auranofin and other gold compounds, Methotrexate, Penicillamine.

Gold Compounds (Auranofin, Aurothioglucose)

“Aurum” is Latin for gold (chemical symbol Au); Auranofin and aurothioglucose are gold compounds, remembered as “AUR- Acts Upon Rheumatoid” arthritis.

Vaccines: Indications and Side Effects

Active immunization (giving antigen so the host develops long-term antibodies) is standard for childhood vaccination schedules. Passive immunization (giving pre-formed immunoglobulins) provides short-term protection, used after recent exposure (tetanus, botulism, hepatitis B, rabies) or for certain travelers. Live attenuated vaccines carry a small risk of causing the disease they protect against; killed/inactivated vaccines do not. Allergic reactions are possible with any vaccine.

Chemotherapy and Secondary Cancer Risk

Certain chemotherapy agents, particularly alkylating agents, carry a long-term risk of secondary malignancies (notably secondary leukemias) in patients successfully treated for an initial cancer.

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Frequently Asked Questions

1. What are the classic teratogenic drugs to know for USMLE?
   Warfarin, thalidomide, anti-epileptic drugs (phenytoin, valproate, carbamazepine), retinoids, ACE inhibitors, lithium, and hormonal agents like OCPs and danazol are the major categories tested.
2. What causes drug-induced pulmonary fibrosis?
   Gold, bleomycin, busulfan, BCNU (carmustine), amiodarone, nitrofurantoin, methotrexate, and methysergide are the classic causes, remembered as “Go BAN Me.”
3. How do you tell physostigmine and neostigmine apart?
   Physostigmine is lipid-soluble, natural, well-absorbed orally, and crosses the blood-brain barrier, used for anticholinergic toxicity. Neostigmine is water-soluble, synthetic, poorly absorbed orally, and doesn’t cross the blood-brain barrier, used for myasthenia gravis.
4. What’s the difference between edrophonium and pyridostigmine in myasthenia gravis?
   Edrophonium is short-acting and used for diagnosis. Pyridostigmine is longer-acting and used for ongoing symptom management.

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Want to Know More?

These are just a few of the mnemonics our community has put together across cardiovascular, CNS, antimicrobial, and endocrine pharmacology. Visit our USMLE student community to find more, share your own, or ask a question about a topic you’re stuck on.