USMLE Vault · Divine Intervention Pharmacology
Step 2 / 3 · Study Guide
Pharmacology System

Pharmacology

12 episodes · 4 Rapid Review inline · Divine Intervention Podcast

High-yield pharmacology for USMLE Step 2/3 — ANS receptors, cardiovascular drugs, anti-infectives, endocrine pharmacology, toxicology, and drug interactions, extracted from Divine Intervention and organized by clinical cluster for exam performance.

3 episodes
Cardiovascular Pharmacology
Cardiovascular drugs dominate Step 2/3 pharmacology. The mechanistic hierarchy — preload vs afterload reduction, rate vs rhythm control, vasospasm vs thrombosis — organizes every choice. Know when nitrates hurt (hypotension), why beta blockers help in HF but worsen vasospasm, and which QT-prolonging drugs trigger torsades.
EP432
Pharmacology Blitz — Cardiovascular Drugs
  • Nitrates — mechanism: Venodilators → ↓ preload → ↓ cardiac workload. Used for MI chest pain, angina, acute decompensated HF. Classic side effect: hypotension + reflex tachycardia. Nitrates + sildenafil = lethal hypotension (both dilate vessels)
  • Hydralazine: Direct arteriolar dilator → ↓ afterload. Used in HF (with isosorbide dinitrate for Black patients — BiDil), hypertension in pregnancy. Drug-induced lupus (+ procainamide, isoniazid, quinidine)
  • ACE inhibitors vs ARBs: Both improve survival in HF and diabetic nephropathy. ACEi → cough (bradykinin accumulation) and angioedema. ARBs = no cough. Both cause hyperkalemia + rising creatinine (especially with NSAIDs). Contraindicated in pregnancy (fetal renal agenesis)
  • Spironolactone / eplerenone: Aldosterone antagonists (K-sparing diuretics). Improve survival in HF. Side effect: gynecomastia (spironolactone, not eplerenone). Hyperkalemia especially with ACEi + ARB
  • Loop diuretics (furosemide): ↓ preload, reduce pulmonary edema in acute HF. Cause ototoxicity (especially with aminoglycosides), hypokalemia, metabolic alkalosis. Give with KCl supplementation
  • Digoxin: ↑ contractility (inhibits Na/K-ATPase → ↑ intracellular Ca) + slows AV node (vagotonic). Used in HFrEF + AFib rate control. Narrow therapeutic index — toxicity: yellow-green vision, nausea, arrhythmias. Hypokalemia ↑ digoxin toxicity. Treat toxicity with digoxin Fab fragments
NitratesACE InhibitorsDigoxinHeart Failure DrugsSpironolactoneDrug-Induced Lupus

Heart Failure Drug Hierarchy

Drug ClassMechanismKey BenefitKey Toxicity
ACE inhibitors (lisinopril)↓ Ang II → ↓ afterload + preloadImprove survival HFrEFCough, angioedema, hyperkalemia, teratogen
ARBs (losartan)Block AT1 receptorSame as ACEi; use if ACEi coughNo cough; same renal/K risks
Sacubitril/valsartan (Entresto)ARB + neprilysin inhibitor → ↑ BNPMortality benefit over ACEi alone in HFrEFHypotension; never combine with ACEi
Beta blockers (carvedilol, metoprolol, bisoprolol)↓ catecholamine toxicityImprove survival in stable HFAvoid acute decompensation; bradycardia
Spironolactone / eplerenoneAldosterone antagonistSurvival benefit, esp. post-MI HFGynecomastia (spirono), hyperkalemia
SGLT-2 inhibitors (empagliflozin)Block renal glucose reabsorptionImprove HF outcomes independent of diabetesUTI, DKA (euglycemic), genitourinary infections
Hydralazine + isosorbide dinitrateArteriolar + venous dilationAlternative to ACEi; preferred in Black patientsReflex tachycardia, drug-induced lupus (hydralazine)
Drug-Induced Lupus — The HIQP Mnemonic

Drugs causing SLE-like syndrome (positive ANA, anti-histone antibodies): Hydralazine, Isoniazid, Quinidine, Procainamide. Anti-histone antibodies = drug-induced lupus (contrast with anti-dsDNA = real SLE, anti-Sm = specific for SLE). Syndrome resolves on drug discontinuation.

Digoxin Toxicity — Recognition and Management

  • Symptoms: Nausea/vomiting, yellow-green visual halos, bradycardia, AV block, ventricular arrhythmias
  • Precipitating factors: Hypokalemia (most important — K competes with digoxin for Na/K-ATPase), hypomagnesemia, renal failure (digoxin renally cleared)
  • EKG: Scooped ST depression ("Salvador Dali mustache"), bradycardia, heart block
  • Treatment: Stop digoxin; correct hypokalemia; digoxin-specific Fab antibody fragments for severe toxicity. Atropine for bradycardia
Nitrate + PDE-5 Inhibitor — Absolute Contraindication

Sildenafil, tadalafil (PDE-5 inhibitors) prevent cGMP breakdown → sustained vasodilation. Nitrates also work via cGMP. Combined effect: catastrophic hypotension. Never co-administer. If patient took sildenafil and presents with MI, cannot give nitrates — use morphine and other analgesics only.

EP609
ANS Drugs for Step 2 & 3 — Beta Blockers & Alpha Agents
  • Selective beta-1 blockers (A to M): Atenolol, esmolol, acebutolol, metoprolol — heart rate control, HF survival (carvedilol, bisoprolol, metoprolol). Propranolol (non-selective) = migraine prophylaxis, essential tremor, thyroid storm (inhibits 5'-deiodinase), portal hypertension (varices)
  • Alpha-1 blockers (prazosin, tamsulosin): BPH (open bladder neck), PTSD nightmares (prazosin), pheochromocytoma pre-op (block alpha before beta — risk of unopposed alpha if reversed). Phenoxybenzamine (irreversible alpha blocker) = pheo pre-op preferred
  • Alpha-2 agonists (clonidine, methyldopa): Clonidine = antihypertensive (rebound hypertension if stopped), third-line ADHD. Methyldopa = safe antihypertensive in pregnancy (with hydralazine, labetalol, nifedipine)
  • Mirtazapine (alpha-2 blocker): Raises NE (disinhibition); antidepressant without sexual side effects; causes sedation + weight gain → good for anorexic depressed patients
  • Beta blockers — glaucoma: Timolol, betaxolol → ↓ aqueous humor production (sympathetics drive humor production). Apraclonidine/brimonidine (alpha-2 agonists) also ↓ aqueous humor
  • Carvedilol / labetalol: Alpha + beta blockers. Carvedilol = HF. Labetalol = safe in pregnancy, hypertensive emergencies
Beta BlockersAlpha BlockersClonidinePrazosinPropranololPheochromocytoma

Beta Blocker Selection — A to M Rule

DrugSelectivityHY Clinical Use
Atenolol, metoprolol, bisoprololBeta-1 selectiveHF survival, MI, rate control AFib
EsmololBeta-1 selective, ultra-shortIntraoperative HTN, thyroid storm (IV)
PropranololNon-selective (B1+B2)Migraine prophylaxis, essential tremor, thyroid storm, varices
Timolol / betaxololNon-selective / B1Open-angle glaucoma (topical)
CarvedilolAlpha-1 + B1 + B2Heart failure (mortality benefit)
LabetalolAlpha-1 + B1 + B2Pregnancy HTN, hypertensive emergencies
Pheochromocytoma — Alpha Before Beta (Mandatory)

Always give alpha blockade (phenoxybenzamine or prazosin) BEFORE any beta blocker in pheochromocytoma management. Beta blockers alone → unopposed alpha-1 stimulation → paradoxical hypertensive crisis. Rule: alpha first, then beta, never beta alone.

Antihypertensives Safe in Pregnancy

  • Methyldopa — alpha-2 agonist; long safety record
  • Hydralazine — arteriolar dilator; first-line for hypertensive emergencies in pregnancy
  • Labetalol — alpha+beta blocker; safe, widely used
  • Nifedipine — calcium channel blocker (dihydropyridine); safe; also used as tocolytic >32 weeks
  • Contraindicated: ACEi, ARBs (fetal renal agenesis), thiazides (teratogenic)
EP398
Pharmacology Scenarios — Coronary Vasospasm, QT Prolongation & TCA Toxicity
  • Cocaine / meth → coronary vasospasm: ↑ catecholamines at adrenergic synapses → coronary vasoconstriction → MI with minimal atherosclerosis (30% stenosis on cath). Meth = prominent hallucinations (differentiator from cocaine)
  • Sumatriptan / ergotamine: Net vasoconstrictors (used for migraines) → contraindicated in variant angina, Raynaud's, prior MI. Vasospastic coronary disease is the mechanism
  • Variant angina (Prinzmetal): Female smoker, chest pain worse at rest (especially at night), normal coronaries on cath. Treat with calcium channel blockers (both classes). Avoid beta blockers (unopposed alpha → vasoconstriction worsens) and sumatriptan
  • QT prolongation → Torsades de Pointes: Mechanism = sodium OR potassium channel blockade. Drugs: TCAs, ziprasidone (antipsychotic with strongest QT effect), ondansetron (Zofran), macrolides, fluoroquinolones, azole antifungals. Hypokalemia and hypomagnesemia worsen risk
  • TCA toxicity (anti-HAM): Anti-H1 (sedation), Anti-Alpha-1 (orthostatic hypotension), Anti-Muscarinic (anticholinergic syndrome). Also: sodium channel blockade → wide QRS → treat with sodium bicarbonate. Widened QRS is the telltale EKG sign
  • Vancomycin — Red Man Syndrome: Histamine release → cutaneous flushing, not allergic reaction. Reduce infusion rate + pretreat with antihistamine. IV antibiotics required for endocarditis/osteomyelitis (not oral)
Coronary VasospasmQT ProlongationTorsadesTCA ToxicityRed Man SyndromeVariant Angina

QT-Prolonging Drugs — Master List

Drug ClassExamplesKey Note
AntipsychoticsZiprasidone (strongest), haloperidol, thioridazineZiprasidone = highest QT risk of all antipsychotics
Tricyclic antidepressantsAmitriptyline, nortriptylineAlso wide QRS via Na+ channel blockade → NaHCO3 tx
5-HT3 antagonistsOndansetron (Zofran)High-dose IV; avoid in congenital long QT
Macrolide antibioticsAzithromycin, erythromycinAzithromycin Z-pack + cardiac history = concern
FluoroquinolonesCiprofloxacin, levofloxacin, moxifloxacinMoxifloxacin highest QT risk in class
Azole antifungalsFluconazole, voriconazoleAlso CYP3A4 inhibitors → can raise levels of other QT drugs
Antiarrhythmics (class Ia, III)Quinidine, sotalol, amiodaroneAmiodarone = many side effects (thyroid, lung, liver, cornea, skin)
TCA Toxicity — Anti-HAM Framework

H = antiHistamine → sedation
A = anti-Alpha-1 → orthostatic hypotension (especially combined with CCBs, nitrates)
M = antiMuscarinic → anticholinergic syndrome (hot, dry, flushed, tachycardic, confused)
PLUS sodium channel blockade → wide QRS on EKG → treat with IV sodium bicarbonate (alkalinize + provide Na+)

Flush Reactions — Differentiating Causes

Multiple drugs cause cutaneous flushing: Niacin (prostaglandin-mediated; reduce with aspirin), Vancomycin (Red Man — histamine; slow infusion), Adenosine (used for SVT/stress test), Nitrates, CCBs (especially dihydropyridines), Echinocandins (caspofungin, micafungin). Stable vitals = infusion reaction, not anaphylaxis.

3 episodes
Autonomic & CNS Pharmacology
Autonomic pharmacology on Step 2/3 is applied physiology — understanding alpha vs beta receptors explains everything from anaphylaxis treatment to PTSD management to glaucoma therapy. Anesthetic complications have gained emphasis since the November 2020 USMLE changes: malignant hyperthermia, opioid respiratory depression, and OSA management are now regularly tested.
EP609
ANS Receptors — Full Map for Step 2 & 3
  • Alpha-1 (vessels, bladder neck, eye): Stimulate → vasoconstriction (↑ afterload + preload), ↓ urination (bladder neck closes), mydriasis. Reflex bradycardia follows BP rise. Phenylephrine/ephedrine = alpha-1 agonists (nasal congestion, intraoperative hypotension)
  • Alpha-2 (presynaptic sympathetic neurons): Stimulate → ↓ NE production. Clonidine (agonist) = antihypertensive, PTSD, ADHD (3rd line). Alpha-2 agonists in eye (apraclonidine, brimonidine) = ↓ aqueous humor
  • Beta-1 (heart + JG cells): Stimulate → ↑ HR + ↑ contractility + ↑ renin. Thyroid hormone inserts more beta-1 receptors → hyperthyroid tachycardia + AFib. Dobutamine (beta-1 agonist) = cardiogenic shock, pharmacologic stress test
  • Beta-3 (bladder detrusor): Stimulate → detrusor relaxation → prevents urination. Mirabegron (beta-3 agonist) = urge incontinence (overactive bladder). Fight-or-flight: you don't pee → beta-3 stops detrusor
  • Muscarinic (DUMBELS locations): Airway = bronchoconstriction; AV node = slow conduction; bladder = detrusor contraction; GI = ↑ motility; eye = miosis. Muscarinic antagonists (oxybutynin, tolterodine) = urge incontinence. Anticholinergics → delirium in elderly
  • Nicotinic receptors: Target of autoantibodies in myasthenia gravis. Target of neuromuscular blocking agents (succinylcholine, rocuronium). Pyridostigmine (AChEI) = MG treatment. Physostigmine = atropine overdose reversal
ANS ReceptorsMirabegronMuscarinicNicotinicDobutamineOrganophosphate

ANS Receptor Master Table

ReceptorLocationStimulation EffectHY Drug
Alpha-1Vessels, bladder neck, eye (dilator pupillae)Vasoconstriction, bladder neck closes, mydriasisPhenylephrine (agonist); Prazosin (blocker)
Alpha-2Presynaptic sympathetic nerve terminals↓ NE release (inhibitory Gi)Clonidine (agonist = ↓ BP); Mirtazapine (blocker = ↑ NE)
Beta-1Heart (SA/AV node, myocardium), JG cells (kidney)↑ HR, ↑ contractility, ↑ reninDobutamine (agonist); Metoprolol (blocker)
Beta-2Airway smooth muscle, vascular endothelium, uterusBronchodilation, vasodilation, uterine relaxationAlbuterol (agonist); Propranolol (non-selective blocker)
Beta-3Bladder detrusorDetrusor relaxation → hold urineMirabegron (agonist) for urge incontinence
Muscarinic (M2)AV node↓ AV conduction speedAtropine (blocker) for bradycardia
Muscarinic (M3)Bladder, airways, GI, eye (sphincter pupillae)Detrusor contraction, bronchoconstriction, ↑ motility, miosisBethanechol (agonist); Oxybutynin (blocker)
Epinephrine vs Norepinephrine — HY Receptor Distinction

Norepinephrine: Alpha-1 + Alpha-2 + Beta-1. Primary alpha effect = vasoconstriction = drug of choice in septic shock (Levophed).
Epinephrine: Alpha-1 + Alpha-2 + Beta-1 + Beta-2. Beta-2 = bronchodilation → drug of choice in anaphylaxis. NE lacks beta-2 potency — this is why epi, not NE, is used for anaphylaxis.

Cholinergic Toxidrome vs Anticholinergic Toxidrome

Cholinergic (DUMBELS)Anticholinergic (Hot, Mad, Dry, Blind, Tachy)
PupilsMiosis (constriction)Mydriasis (dilation)
HeartBradycardiaTachycardia
SecretionsSLUDGE (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis)Dry mouth, dry skin, urinary retention
SkinSweating, diaphoresisHot, flushed, dry
CauseOrganophosphates, nerve gas, AChEI overdoseAtropine OD, diphenhydramine, TCAs, antipsychotics
TreatmentAtropine (blocks muscarinic) + Pralidoxime (regenerates AChE)Physostigmine (for atropine OD)
EP475
Beta-2 and Beta-3 Receptors — Clinical Pharmacology
  • Albuterol (SABA) — key integrations: Bronchodilation for asthma/COPD. Also stimulates Na/K-ATPase → shifts K+ intracellularly → treats hyperkalemia (after calcium gluconate stabilizes myocardium). Continuous albuterol → hypokalemia (mechanism = K+ redistribution, not renal loss)
  • Long-acting beta-2 agonists (LABA): Salmeterol, formoterol → 3rd rung in asthma ladder (add after SABA + inhaled corticosteroid). Never use LABA monotherapy in asthma without ICS (safety concern)
  • Asthma management ladder: SABA (albuterol) → add ICS (budesonide, fluticasone) → add LABA → consider biologic (dupilumab for eosinophilic asthma)
  • Tocolysis hierarchy: <32 weeks → indomethacin (COX inhibitor; prostaglandins cause uterine contraction); >32 weeks → nifedipine (CCB; Ca needed for contraction). Terbutaline (beta-2 agonist) = historical; avoid on exams if indomethacin or nifedipine are available
  • Beta blocker overdose → glucagon antidote: Beta blockers ↓ cyclic AMP intracellularly. Glucagon receptor is stimulatory Gp-coupled receptor (different from adrenergic receptors) → raises cAMP via separate pathway → reverses beta blocker bradycardia and hypotension. Glucagon also relaxes esophagus (food impaction)
  • Mirabegron (beta-3 agonist): Relaxes detrusor → treats urge incontinence. Alternative to antimuscarinics (oxybutynin); no anticholinergic side effects; good option in elderly
AlbuterolTocolysisHyperkalemiaAsthma LadderBeta Blocker ODGlucagon

Hyperkalemia Management — Stepwise

StepDrugMechanismOnset
1 — Stabilize myocardiumCalcium gluconateRaises threshold potential (membrane stabilization)Minutes
2a — Shift K+ intracellularlyAlbuterolBeta-2 → stimulates Na/K-ATPase → K+ enters cells15-30 min
2b — Shift K+ intracellularlyInsulin + dextroseInsulin stimulates Na/K-ATPase; glucose prevents hypoglycemia15-30 min
3 — Remove K+ from bodyFurosemide (if UO intact)Loop diuretic → renal K+ excretionHours
4 — Remove K+ from bodyKayexalate or patiromerBinds K+ in gut; excreted in stoolHours to days
5 — EmergencyDialysisDirectly removes K+ from bloodFastest definitive removal
Tocolytic Decision Tree

<32 weeks gestation: Indomethacin (NSAID → ↓ prostaglandins → ↓ uterine contractions). Risk if >32 weeks: closes ductus arteriosus prematurely.
>32 weeks gestation: Nifedipine (calcium channel blocker → ↓ myometrial Ca → relaxation). Safe past 32 weeks, no ductus risk.
Terbutaline (beta-2 agonist): Exam distractor — only pick if indomethacin and nifedipine are NOT available.

EP385
Anesthetic Complications and The USMLEs
  • Most common cause of anesthetic complications: Human error (wrong drug, wrong dose). Prevention: color-coded syringes, barcode verification
  • Malignant hyperthermia: Autosomal dominant (ryanodine receptor mutation → uncontrolled Ca release from SR). Triggered by depolarizing NMBAs (succinylcholine) or volatile inhaled anesthetics. Presentation: fever (105°F+), rigidity, hyperkalemia, rhabdomyolysis → AKI. Treat with dantrolene (ryanodine receptor antagonist = Ca channel blocker)
  • Opioid-induced respiratory depression post-op: Somnolent, RR 5, PCO2 ↑, PaO2 ↓ → respiratory acidosis. Diagnosis: opiate-induced respiratory depression (RASS scale for monitoring). Treat: naloxone (opioid antagonist). NOT reintubation first — give naloxone first
  • OSA in anesthesia: Screen with STOP-BANG questionnaire. Use patient's CPAP/BiPAP while hospitalized. Prefer regional over general anesthesia. Limit opioids (additive respiratory depression)
  • Beta blockers + surgery: Continue if already on them. Do NOT start de novo in perioperative period (↑ morbidity + mortality). Anemia + beta blockers = dangerous combination (anemia ↑ cardiac demand; beta blockers blunt compensatory HR increase)
  • Tension pneumothorax (central line complication): Absent breath sounds unilaterally, hypotension, tracheal deviation. Treat: needle decompression (needle thoracostomy) → then chest tube (tube thoracostomy). If only chest tube available on exam → pick chest tube
Malignant HyperthermiaDantroleneNaloxoneOSA AnesthesiaTension PneumoSTOP-BANG

Malignant Hyperthermia vs NMS vs Serotonin Syndrome

Malignant HyperthermiaNeuroleptic Malignant SyndromeSerotonin Syndrome
TriggerSuccinylcholine, volatile anestheticsAntipsychotics (especially typical)Serotonergic combinations (SSRI + MAOI, linezolid, methylene blue, meperidine)
SettingOperating room, intraoperativeHospital, new antipsychotic or dose increaseAny setting after combining serotonergic drugs
RigiditySevere ("lead pipe")Severe ("lead pipe")Hyperreflexia + clonus (not true rigidity)
TemperatureVery high (>105°F)Very highHigh but usually less extreme
TreatmentDantrolene (ryanodine antagonist)Dantrolene + bromocriptine + stop antipsychoticCyproheptadine (5-HT2 antagonist) + benzos
GeneticsAD — ryanodine receptor mutationNot geneticNot genetic
Malignant Hyperthermia — Electrolyte Consequence

As muscle cells lyse (rhabdomyolysis), intracellular K+ floods into serum → hyperkalemia. Myoglobin release → acute tubular necrosis → AKI → worsens hyperkalemia. Also: metabolic acidosis (anaerobic metabolism). NBME may ask: "most likely electrolyte abnormality in MH?" → Answer: hyperkalemia.

Pre-operative Risk Assessment

  • >4 METs: Low cardiac risk; no formal cardiac work-up needed before elective surgery
  • High cardiac risk factors: Ischemic heart disease, HF, DM, CKD, age >65
  • Post-MI timing: Delay elective surgery ≥60 days after MI
  • Quit smoking: Minimum 8 weeks before surgery
  • Prone surgery vision loss: Eyes lower than heart → ↑ intraocular pressure → optic ischemia → reverse Trendelenburg (head higher than feet) to prevent
  • RA pre-op: Get cervical X-ray to screen for atlanto-axial (C1-C2) instability (also: Down syndrome, ankylosing spondylitis)
12 episodes
Also Covered In Other Episodes
Divine’s rapid-review episodes mix several systems into one recording. These episodes are filed under another system but contain a substantial Pharmacology segment. The title names the whole episode; the bullets are the Pharmacology portion only.
RR 64 EP336EP336
Rapid Review 64 - Optic Neuritis, Cholinesterase Inhibitors, Absence Seizures, Wilson Disease
Cross-listed. This episode is filed under Hematology/Oncology. Below is only its Pharmacology content.
  • Acetylcholinesterase inhibitors approved for Alzheimer disease: donepezil, galantamine, rivastigmine
  • Pyridostigmine for myasthenia gravis, outcompeting anti-nicotinic acetylcholine receptor antibodies
  • Physostigmine for atropine overdose and the anticholinergic toxidrome (tachycardia, mydriasis, non-infectious fever)
  • Atropine first then pralidoxime for organophosphate poisoning and cholinergic toxidrome
  • Neostigmine for postoperative ileus and overflow incontinence; bethanechol and carbachol as muscarinic agonist alternatives
  • Ethosuximide as a T-type calcium channel blocker, tested as a mechanism-based derivative answer
RR 134 EP638EP638
Rapid Review 134 - Toxic Megacolon, Tinea Corporis, Asherman Syndrome, Multiple System Atrophy
Cross-listed. This episode is filed under Infectious Disease. Below is only its Pharmacology content.
  • Ethacrynic acid instead of furosemide for CHF exacerbation in a patient with severe sulfa allergy; it is the most ototoxic loop diuretic
  • Other ototoxic drugs: vancomycin, cisplatin, and aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin)
  • Meglitinides (repaglinide, nateglinide) as sulfa-free, faster-acting alternatives to sulfonylureas (glyburide, glipizide, glimepiride)
  • Dermatophyte treatment: topical azole for tinea corporis, but systemic terbinafine or griseofulvin for tinea capitis and onychomycosis because keratin penetration is needed
  • Griseofulvin as a CYP450 inducer, alongside rifampin, barbiturates, phenytoin, and St. John's wort
RR 115 EP536EP536
Rapid Review 115 - Presbycusis & Ototoxic Drugs, Nicotine Withdrawal, Migraine, MAOI Crisis
Cross-listed. This episode is filed under MSK & Rheumatology. Below is only its Pharmacology content.
  • Drug-induced ototoxicity across many vignettes: aminoglycosides (gentamicin, tobramycin, neomycin, amikacin), cisplatin, loop diuretics such as ethacrynic acid, high-dose aspirin, and vancomycin
  • Bupropion for smoking cessation and its contraindications: seizure disorders and eating disorders; varenicline as a nicotinic partial agonist with neuropsychiatric caution
  • Migraine treatment pharmacology: triptans, NSAIDs as an acute alternative, and prophylaxis with beta blockers, TCAs, topiramate or calcium channel blockers matched to comorbidities
  • MAOI tyramine crisis mechanism: unbroken tyramine displaces catecholamines from synaptic vesicles causing hypertensive crisis and brain bleed
  • Drug causes of skin flushing: vancomycin histamine release, adenosine, niacin, and dihydropyridine calcium channel blockers with peripheral edema
RR 130 EP622EP622
Rapid Review 130 - Carbamazepine SIADH, HCM, Beta Blocker Uses, Renal Vein Thrombosis
Cross-listed. This episode is filed under MSK & Rheumatology. Below is only its Pharmacology content.
  • Carbamazepine toxicities: SIADH with hyponatremia and agranulocytosis with febrile neutropenia; also used for trigeminal neuralgia
  • Comprehensive beta blocker indication review: heart failure, HCM, stable angina, glaucoma, aortic dissection, essential tremor, akathisia, performance-type social anxiety, migraine prophylaxis, AFib rate control
  • Beta blocker contraindications: acute CHF exacerbation, pheochromocytoma and cocaine intoxication without prior alpha blockade
  • Beta blockers in glaucoma by reducing sympathetically driven aqueous humor production
RR 70 EP369EP369
Rapid Review 70 - Esophageal Rupture, Exploratory Laparotomy, Small Bowel Obstruction
Cross-listed. This episode is filed under OB/GYN. Below is only its Pharmacology content.
  • Drugs that cause ileus/small bowel obstruction on exams: opioids and anticholinergics
  • Specific anticholinergic offenders named: diphenhydramine, chlorpromazine and tricyclic antidepressants
  • TCA anti-HAM side effects: antihistamine sedation, anti-alpha-1 orthostatic hypotension, antimuscarinic effects
  • Calcium channel blockers such as amlodipine impairing GI smooth muscle and myenteric plexus function
  • Anticholinergic drugs also causing delirium
RR 63 EP335EP335
Rapid Review 63 - Tularemia, Toxic Shock Syndrome, Q Fever, Melioidosis, CMV
Cross-listed. This episode is filed under Gastrointestinal. Below is only its Pharmacology content.
  • Doxycycline, aminoglycoside, or ciprofloxacin for tularemia; ciprofloxacin also for pyelonephritis and anthrax on NBME exams
  • Ceftazidime (third-gen cephalosporin with pseudomonal coverage) plus prolonged Bactrim for melioidosis
  • Doxycycline first-line for Rocky Mountain spotted fever in everyone including children under 8 and pregnant patients; chloramphenicol as second line
  • Chloramphenicol toxicities: agranulocytosis requiring white count monitoring, and gray baby syndrome
  • Ganciclovir requires UL97 kinase activation to inhibit DNA polymerase; UL97 mutation causes resistance, so switch to foscarnet, a pyrophosphate analog
  • Vasopressor sequence in septic shock: norepinephrine, then vasopressin, then epinephrine
RR 122 EP601EP601
Rapid Review 122 - Iatrogenic Cushing Syndrome, SIADH, DiGeorge & Hyperparathyroidism
Cross-listed. This episode is filed under Gastrointestinal. Below is only its Pharmacology content.
  • Patients on long-term corticosteroids need bisphosphonate therapy because steroids activate osteoclasts and cause osteoporosis
  • PPI coverage is reasonable in chronic steroid users to prevent peptic ulcer disease
  • Chronic steroids cause immunosuppression and Pneumocystis jirovecii pneumonia in non-HIV patients
  • Chlorpropamide is a sulfonylurea with a strong SIADH association, tested because it does not sound like glyburide/glipizide/glimepiride
EP298
Esophageal Rings & Webs, Zenker Diverticulum, Peptic Ulcer Disease, Zollinger-Ellison
Cross-listed. This episode is filed under Gastrointestinal. Below is only its Pharmacology content.
  • NSAIDs cause gastric ulcers by inhibiting cyclooxygenase and eliminating protective prostaglandins
  • PPIs treat Zollinger-Ellison syndrome by blocking acid formation
  • Metronidazole inhibits acetaldehyde dehydrogenase, producing a disulfiram-like reaction with alcohol
  • Octreotide (somatostatin analog) and pegvisomant (GH receptor antagonist) for acromegaly
RR 81 EP408EP408
Rapid Review 81 - Ascending Cholangitis, Cholecystitis vs Choledocholithiasis, ERCP
Cross-listed. This episode is filed under Gastrointestinal. Below is only its Pharmacology content.
  • Empiric IV regimen for acute/ascending cholangitis: ampicillin plus gentamicin plus metronidazole
  • Ampicillin and gentamicin cover gram negatives such as E. coli, the typical GI tract pathogens
  • Metronidazole is added specifically for anaerobic coverage
RR 72 EP380EP380
Rapid Review 72 - Herpetic Whitlow, Aminoglycoside Toxicity, TMP-SMX, G6PD Deficiency
Cross-listed. This episode is filed under Emergency Medicine. Below is only its Pharmacology content.
  • Acyclovir and ganciclovir as DNA-dependent DNA polymerase inhibitors, and how the NBME writes these 'derivative answers'
  • Reverse transcriptase inhibitors reframed as inhibitors of an RNA-dependent DNA polymerase; rifampin reframed as a DNA-dependent RNA polymerase inhibitor
  • When to choose oral versus IV therapy on exams: only for severe illness or inability to tolerate oral intake
  • Aminoglycoside ototoxicity, nephrotoxicity and neuromuscular blockade (avoid in myasthenia gravis, ALS, Lambert-Eaton); shared oto/nephrotoxicity with vancomycin, ethacrynic acid and cisplatin
  • TMP-SMX mechanism (dihydropteroate synthetase and dihydrofolate reductase inhibition), bone marrow suppression, and ENaC blockade causing hyperkalemia
RR 85 EP420EP420
Rapid Review 85 - Parvovirus B19, Beckwith-Wiedemann, ACE Inhibitors, Renal Artery Stenosis
Cross-listed. This episode is filed under Pediatrics. Below is only its Pharmacology content.
  • Mechanism of ACE inhibitors: blocked angiotensin I to II conversion, loss of efferent arteriolar constriction, reduced aldosterone
  • Predictable ACE inhibitor lab changes -- minor creatinine bump, mild hyperkalemia, metabolic acidosis -- and why aldosterone loss causes proton retention
  • Using the magnitude of the ACE inhibitor/ARB response as the clue to underlying renal artery stenosis (minor bumps normal, massive bumps abnormal)
  • Insulin plus glucose in hyperkalemia via increased Na/K-ATPase activity, and calcium gluconate first for myocardial stabilization
EP349
Psych Pharm Review - Antidepressants, Antipsychotics, Mood Stabilizers, EPS, Benzodiazepines
Cross-listed. This episode is filed under Psychiatry. Below is only its Pharmacology content.
  • Atypical antidepressants by mechanism and niche: bupropion (NDRI, smoking cessation, seizure threshold), mirtazapine (alpha-2 blocker, sedation, weight gain), trazodone (priapism treated with intracavernosal phenylephrine)
  • SSRI class effects (sexual dysfunction, SIADH, discontinuation syndrome except fluoxetine) and SNRI class effects (raised blood pressure, duloxetine/milnacipran for fibromyalgia and diabetic neuropathy)
  • TCA toxicity: wide QRS from sodium channel blockade treated with sodium bicarbonate, plus anti-HAM (antihistamine, anti-alpha-1, antimuscarinic) side effects
  • MAOIs and tyramine-rich foods causing hypertensive crisis
  • Lithium side effect profile (tremor, nephrogenic diabetes insipidus blocked by amiloride, hypothyroidism, Ebstein anomaly) and clozapine monitoring for agranulocytosis and myocarditis
3 episodes · 1 Rapid Review
Anti-infective Pharmacology
Anti-infective pharmacology on Step 2/3 focuses on three axes: mechanism (cell wall vs protein synthesis vs DNA), resistance patterns, and toxicities. The G6PD/oxidative hemolysis connection ties anti-infective drugs (dapsone, TMP-SMX, nitrofurantoin, primaquine) to the hematology section. Pain control drugs — acetaminophen, NSAIDs, opioids — are tested through mechanism-based clinical scenarios rather than raw fact recall.
EP484
Step 2 & 3 Drugs Series 1 — Pain Control (APAP, NSAIDs, Opioids)
AcetaminophenN-AcetylcysteineNSAIDsAspirin ToxicityOpioidsNaloxone

NSAID Clinical Uses — HY Summary

ConditionDrugMechanism
Acute MI — antiplateletAspirin (irreversible COX-1 → ↓ TXA2)First drug in STEMI protocol
Kawasaki diseaseAspirin + IVIGOnly pediatric indication for aspirin (Reye's risk otherwise)
Patent ductus arteriosus (close)Indomethacin↓ PGE2 → ductus constricts; avoid >32 weeks gestation
Primary dysmenorrheaNSAIDs↓ prostaglandin-mediated myometrial contractions
Acute gout (first-line)Indomethacin or naproxenAnti-inflammatory; colchicine is alternative
Acute pericarditisAspirin or ibuprofen + colchicineAnti-inflammatory combination reduces recurrence
Tocolysis <32 weeksIndomethacin↓ prostaglandins → uterine relaxation
Osteoarthritis (step 2)NSAIDs after acetaminophen failsAdd GI protection (PPI) if needed
Aspirin Toxicity — Both Acid-Base Disorders Simultaneously

Salicylate directly stimulates the respiratory center → hyperventilation → blows off CO2 → respiratory alkalosis (PCO2 ↓).
Acetylsalicylic acid itself is an acid + uncouples oxidative phosphorylation → high anion gap metabolic acidosis (bicarb ↓).
Both occur TOGETHER. Common wrong answer: "respiratory alkalosis only." Do not fall for this.

Opioid Toxidrome vs Treatment

RR 73EP382
G6PD Deficiency, Oxidative Drug Toxicity & CGD
G6PD DeficiencyOxidative HemolysisCyanide PoisoningCGDHeinz BodiesHydroxocobalamin

Three Confusing Drug Toxicities — Differentiating Features

G6PD HemolysisMethemoglobinemiaCyanide Poisoning
Hemoglobin level↓ (anemia)Normal (qualitative defect)Normal
Key lab finding↑ LDH, ↓ haptoglobin, Coombs (−)Chocolate-brown blood; perioral cyanosisHigh anion gap lactic acidosis
O2 responseResponds to O2Does NOT respond to O2Responds to O2 (partial)
Speed of presentationHours after exposureHours after exposureMinutes — rapidly fatal
TreatmentStop offending drug; supportiveMethylene blue; vitamin CHydroxocobalamin (1st line); amyl nitrate + thiosulfate (2nd)
Classic exposureTMP-SMX, dapsone, fava beans, primaquineBenzocaine, lidocaine, dapsone, TMP-SMX, nitritesNitroprusside, house fire, apricot seeds
Methemoglobinemia — Methylene Blue Caveat

Methylene blue is the treatment for methemoglobinemia. However, methylene blue is also a potent MAOI. Do NOT give methylene blue to a patient on SSRIs, MAOIs, linezolid, TCAs, or trazodone → risk of serotonin syndrome. NBME clue: patient gets methylene blue for methemoglobin then develops myoclonus/agitation → serotonin syndrome from MAOI effect of methylene blue.

EP387
Adverse Drug Reactions for Step 2CK/3
AminoglycosidesAmphotericin BStevens-JohnsonAgranulocytosisFluoroquinolonesTetracyclines

High-Yield Adverse Drug Reactions — Master Table

DrugToxicityKey Detail
AminoglycosidesNephrotoxicity + ototoxicityMonitor trough; synergistic nephrotox with furosemide
VancomycinRed Man Syndrome (histamine); nephrotoxicitySlow infusion; pre-treat with antihistamine; not anaphylaxis
Amphotericin BNephrotoxicity + ↓K+ ↓Mg2+; infusion reactionsLiposomal form has less kidney toxicity
ClindamycinC. difficile colitis (most common drug)Pseudomembranous colitis; positive toxin assay
ChloramphenicolGray baby syndrome + aplastic anemiaImmature glucuronyl transferase in neonates; banned in US
LinezolidMAOI properties → serotonin syndromeAvoid with SSRIs/MAOIs; also serotonin syndrome risk with methylene blue
FluoroquinolonesTendon rupture, QT prolongation, photosensitivityAvoid in children; especially Achilles tendon in elderly + steroids
TetracyclinesPhotosensitivity, tooth staining (<8y), esophagitisTake upright with water; avoid in pregnancy/children
MetronidazoleDisulfiram-like reaction with alcohol; metallic tasteAvoid alcohol during treatment; covers anaerobes + C. diff + protozoa
IsoniazidPeripheral neuropathy (↓ B6) + hepatotoxicityGive pyridoxine (B6) with INH; slow acetylators at higher risk
RifampinHepatotoxicity; orange discoloration of body fluids; potent CYP3A4 inducerReduces levels of warfarin, OCPs, many drugs
EthambutolOptic neuritis (red-green color blindness)Baseline and periodic visual acuity testing
PyrazinamideHyperuricemia → gout; hepatotoxicityPart of RIPE regimen; check uric acid
Drugs That Require Mandatory Monitoring

Clozapine: ANC (agranulocytosis) — weekly CBC × 6 months, then biweekly
Lithium: Serum levels + TFTs + BMP (narrow therapeutic index; polyuria, tremor, hypothyroidism)
Methotrexate: LFTs (hepatotoxicity) + CBC (bone marrow suppression)
Amiodarone: TFTs, LFTs, PFTs, eye exam (corneal deposits, optic neuropathy)
Hydroxychloroquine: Annual dilated eye exam (retinopathy)

3 episodes · 2 Rapid Review
Endocrine & Metabolic Pharmacology
Endocrine pharmacology integrates physiology, biochemistry, and clinical management. The corticosteroid section covers 50 high-yield facts across indications, side effects, and tapering. GLP-1 agonists and SGLT-2 inhibitors are among the most tested diabetes drugs. Thyroid storm pharmacology tests whether you understand the mechanism of each sequential drug — beta blocker, PTU, SSKI, and steroids — not just which drugs are used.
EP539
50 HY Corticosteroid Facts for Step 1-3
CorticosteroidsHPA AxisStress Dose SteroidsCushing Side EffectsBetamethasoneAdrenal Insufficiency

Corticosteroid Potency Comparison

DrugGlucocorticoid PotencyMineralocorticoid PotencyKey Use
Cortisol (hydrocortisone)1× (reference)Stress dosing, adrenal insufficiency
Prednisone0.8×Autoimmune diseases, asthma
Methylprednisolone0.5×IV for acute exacerbations (MS, COPD)
Dexamethasone25×~0Cerebral edema, croup (1 dose), meningitis (with ceftriaxone)
Betamethasone25×~0Fetal lung maturity (<34 weeks)
Fludrocortisone10×125× (strongest mineralocorticoid)Adrenal insufficiency (mineralocorticoid replacement), orthostatic hypotension
Post-Op Adrenal Insufficiency After Cushing Adenoma Removal

Adrenal adenoma makes excess cortisol → suppresses ACTH → contralateral normal adrenal gland atrophies (no ACTH stimulation). After adenoma is removed: no cortisol source + atrophied normal adrenal cannot acutely compensate → adrenal crisis (hypotension, hyponatremia, hyperkalemia). MANDATORY: give stress dose glucocorticoids post-operatively. This is a very common, high-yield USMLE scenario.

Cushingoid Signs — ACTH-Dependent vs ACTH-Independent

RR 97EP466
GLP-1 Agonists, Diabetes Drug Weight Effects & Thyroid Storm Pharmacology
GLP-1 AgonistsSGLT-2 InhibitorsThyroid StormPTU vs MethimazoleAmiodaroneWolff-Chaikoff

Diabetes Drug — Weight & Cardiac Effects

Drug ClassMechanismWeightHF/Cardiac BenefitSpecial Concern
Metformin↓ hepatic gluconeogenesis (biguanide)Neutral/slight lossNeutralHold before contrast (lactic acidosis risk); contraindicated in eGFR <30
GLP-1 agonistsIncretin mimetics → ↑ insulin, ↓ glucagonLossCV benefit (liraglutide)Pancreatitis; medullary thyroid CA; avoid in MEN2
SGLT-2 inhibitorsBlock SGLT-2 → ↑ glucosuriaLossStrong HF + renal protectionUTI, Fournier's gangrene, euglycemic DKA
SulfonylureasClose K+ channels → ↑ insulin releaseGainNeutral/negativeHypoglycemia (avoid in elderly); weight gain
Thiazolidinediones (pioglitazone)PPAR-γ agonist → ↑ insulin sensitivityGain (fluid retention)Worsen HFContraindicated in HF (fluid retention); bladder cancer
DPP-4 inhibitorsBlock GLP-1 degradationNeutralNeutralPancreatitis; saxagliptin → worsens HF
InsulinDirect glucose uptakeGainNeutralHypoglycemia; must adjust in renal failure
Thyroid Storm — Treatment Sequence (MUST Know Order)

Step 1 — Beta blocker (propranolol): Blocks sympathetic surge + inhibits 5'-deiodinase (↓ T4→T3)
Step 2 — PTU: Inhibits thyroperoxidase + 5'-deiodinase (use PTU not methimazole in storm)
Step 3 — SSKI (≥1 hour after PTU): Wolff-Chaikoff effect → ↓ organification → ↓ thyroid hormone synthesis. Give AFTER PTU (if given first, iodide could be used to make more hormone)
Step 4 — Steroids: Treat relative adrenal insufficiency from hypermetabolic state + also inhibit 5'-deiodinase

RR 119EP577
Cushing Syndrome Work-Up & Methotrexate Pharmacology
MethotrexateLeucovorinCushing WorkupFolate DeficiencyHomocysteineAtlanto-axial

Methotrexate Uses — HY Summary

ConditionRationaleKey Note
Rheumatoid arthritisDMARD first-line; modifies disease course (NSAIDs don't)Monitor LFTs + CBC. Folate supplementation recommended
Ectopic pregnancyStops trophoblast division; medical managementOnly if: beta-HCG <5000, no fetal cardiac activity, hemodynamically stable
ChoriocarcinomaExtremely chemosensitiveHigh cure rate; monitor beta-HCG
Psoriasis / PsAAntiproliferative on keratinocytesHepatotoxicity limits long-term use
Leukemia/lymphomaS-phase cytotoxicHigh-dose requires leucovorin rescue
Folate Deficiency vs B12 Deficiency — Lab Differentiation

Folate deficiency (methotrexate, TMP-SMX, phenytoin, alcoholism, malabsorption, pregnancy):
→ ↑ homocysteine, NORMAL methylmalonic acid. No neurologic symptoms.
B12 deficiency (pernicious anemia, vegan diet, terminal ileum disease, Diphyllobothrium latum tapeworm):
→ ↑ homocysteine AND ↑ methylmalonic acid. Neurologic symptoms (subacute combined degeneration of cord).

EP517
Niacin (B3) Deficiency, Pellagra & Clinical Integrations
PellagraNiacin DeficiencyCarcinoid SyndromeHartnup DiseaseMSUDIsoniazid + B6

Pellagra Causes — Clinical Context Table

Vignette ClueDiagnosisMechanism
Immigrant + isoniazid for months + pellagraINH-induced B6 deficiency → ↓ tryptophan hydroxylase activityTryptophan→niacin requires B6 as cofactor → supplement pyridoxine
Young female + Crohn's / IBDMalabsorption of niacin in terminal ileumJejunal/ileal inflammation → ↓ niacin absorption
Alcoholic male + megaloblastic anemia + elevated GGTAlcoholism → ↓ niacin + folate reabsorptionMitochondrial toxin; impairs absorption of multiple vitamins
Flushing + diarrhea + wheezing + carcinoid pellagraCarcinoid syndrome (midgut): 70% tryptophan → serotoninTryptophan diverted; niacin synthesis impaired; check 5-HIAA in urine
Sweet-smelling secretions + aminoaciduriaMaple syrup urine diseaseLeucine buildup → inhibits QPRT → ↓ niacin synthesis
Extensive aminoaciduria (neutral AAs) + photosensitivity rashHartnup diseaseCan't reabsorb neutral amino acids (tryptophan) → pellagra
Niacin Pharmacotherapy (High-Dose)

High-dose niacin raises HDL (most potent HDL-raising drug) and lowers triglycerides. Side effects: prostaglandin-mediated flushing (reduce with aspirin pretreatment), hyperglycemia, hyperuricemia (gout), hepatotoxicity. Now less used since niacin + statin showed no additional CV benefit over statin alone.

3 episodes · 1 Rapid Review
Toxicology & Drug Interactions
Toxicology on Step 2/3 is predominantly recognition + mechanism + antidote. The three confusing poisonings (CO, cyanide, methemoglobinemia) test whether you can use oxygen responsiveness and hemoglobin level to differentiate. Drug interactions are almost always CYP-based (warfarin + azoles, rifampin + OCPs) or pharmacodynamic (serotonin syndrome combinations). Herbal supplements are reliably tested — know the six key herbs and their dangerous interactions.
EP399
The 3 Confusing Poisonings — CO, Cyanide, Methemoglobinemia
Carbon MonoxideCyanide PoisoningMethemoglobinemiaHydroxocobalaminMethylene BlueO2 Response

Three Confusing Poisonings — Quick Comparison

Carbon MonoxideCyanideMethemoglobinemia
MechanismCO displaces O2 from Hb; left shift of O2 curveInhibits Complex IV (cytochrome c oxidase)Fe2+ oxidized to Fe3+ → can't carry O2
Presentation speedGradual (hours)Rapid (minutes)Hours after exposure
Hemoglobin levelNormal (just CO-bound)NormalNormal (qualitative defect)
Key findingCarboxyhemoglobin ↑; hypodense globus pallidusHigh anion gap lactic acidosisPerioral cyanosis; chocolate blood; no O2 response
O2 supplementationHelpful (displaces CO)Partially helpfulNOT helpful (Hb can't bind O2 regardless)
Antidote100% O2 / hyperbaric O2Hydroxocobalamin (1st); amyl nitrate + thiosulfate (2nd)Methylene blue; Vitamin C
Cyanide — Amyl Nitrate Creates Methemoglobin (Intentionally)

Amyl nitrate induces methemoglobinemia (oxidizes Hb Fe2+→Fe3+) — intentionally. Why? Ferric hemoglobin (Fe3+) has high affinity for cyanide and "sequesters" it away from cytochrome c oxidase. This is why you must use carefully — too much methemoglobin causes its own hypoxia (Fe3+ can't carry O2). That's why hydroxocobalamin is preferred (no methemoglobin induction risk).

EP606
Drug Interactions for the USMLEs (Step 1-3)
Warfarin InteractionsCYP InducersSerotonin SyndromeNSAID + ACEiOxytocin HyponatremiaStatin + Fibrate

CYP450 Drug Interactions — Master Table

CategoryDrugsEffect on CYPClinical Consequence
CYP Inducers (↑ metabolism of other drugs)Rifampin, St. John's Wort, carbamazepine, phenytoin, phenobarbital, chronic alcoholUpregulate CYP → faster drug breakdown↓ warfarin, ↓ OCPs, ↓ immunosuppressants, ↓ HIV drugs → treatment failure
CYP Inhibitors (↓ metabolism → ↑ drug levels)Azoles (fluconazole, ketoconazole), macrolides, amiodarone, grapefruit juice, metronidazole, isoniazidBlock CYP → slower breakdown↑ warfarin → bleeding; ↑ statins → rhabdo; ↑ QT drugs → torsades; ↑ immunosuppressants → toxicity
Protein binding displacementSulfonamides + warfarinDisplace warfarin from albumin↑ free warfarin → ↑ INR → bleeding
SSRI — Most Common Drug Cause of Hyponatremia

SSRIs cause SIADH → free water retention → hyponatremia. Most common in elderly women. Also causes: sexual dysfunction (delayed ejaculation/orgasm), serotonin syndrome if combined with other serotonergic drugs, and discontinuation syndrome (taper, don't stop abruptly). Paroxetine has highest discontinuation syndrome risk (short half-life). Fluoxetine has lowest risk (long half-life).

High-Yield Drug Interaction Scenarios

EP608
Herbal Supplements and The USMLEs
St. John's WortSaw PalmettoBlack CohoshKava KavaEphedraLicorice

Herbal Supplement High-Yield Table

SupplementUsed ForKey Toxicity / InteractionStop Before Surgery?
St. John's WortDepression, mood, anxiety, insomniaCYP inducer (↓ warfarin, OCP, cyclosporine); serotonergic → serotonin syndrome with SSRIsYes (CYP effect)
Saw palmettoBPH, decreased libido↓ platelet aggregation → bleedingYES — perioperative bleeding
Ginkgo bilobaMemory enhancement↓ platelet aggregation → bleeding; potentiates aspirinYES — perioperative bleeding
GinsengMemory, energy↓ platelet aggregation; headache, insomnia, GI upsetYES — perioperative bleeding
GarlicCholesterol, cardiovascular, cancer prevention↓ platelet aggregation; contact dermatitis (topical)YES — perioperative bleeding
Black cohoshMenopausal symptoms (hot flashes), PMSSevere hepatotoxicity (oxidative) — right upper quadrant pain in middle-aged woman
Kava kavaAnxiety, insomniaHepatotoxicity (delayed weeks after stopping)
EchinaceaCommon cold, URIsSevere hypersensitivity reactions; GI upset
Ephedra (ephedrine)Weight lossSevere hypertension (alpha-1 agonist)
LicoriceFlavor additive; claimed to lower cholesterolPseudo-hyperaldosteronism: HTN + hypokalemia + metabolic alkalosis (11β-HSD2 inhibition)
4 Herbs That Cause Perioperative Bleeding — Stop Before Surgery

Saw palmetto + the 3 Gs: Ginseng, Garlic, Ginkgo biloba all inhibit platelet aggregation. All four must be stopped before any surgery to reduce bleeding risk. This is tested as both a stand-alone fact (which supplement causes bleeding?) and as a pre-op management scenario (patient on herbal supplement going for elective surgery).

RR 125EP612
Hypercoagulability, OCP Pharmacology & SIADH Drug Causes
OCPsHypercoagulabilityVirchow's TriadFactor V LeidenSIADHSSRIs

OCP Indications and Contraindications

IndicationHow OCPs Help
Contraception↓ FSH/LH → prevents ovulation; thickens cervical mucus
Acne (reproductive-age female)↑ SHBG → ↓ free androgens → ↓ sebum production
PCOSRegulate cycle; ↓ androgen symptoms; ↓ hypercoagulability from anovulation
Endometriosis / adenomyosisSuppress endometrial tissue proliferation and bleeding
Primary dysmenorrhea↓ uterine prostaglandins → ↓ cramping
Perimenopausal managementRegulate cycles and reduce symptoms in late reproductive years
OCP Contraindications — High-Yield List

Absolute contraindications to estrogen-containing OCPs:
• History of DVT/PE or thrombophilia (Factor V Leiden, antiphospholipid)
• Migraine WITH aura (↑ stroke risk)
• Uncontrolled hypertension (>160/100 mmHg)
• Liver disease / hepatocellular adenoma
• Estrogen-sensitive breast cancer
• Smokers >35 years old
• Postpartum <21 days (hypercoagulable period)
→ Use progestin-only pills ("mini-pill") or IUD in these patients

SIADH — Diagnosis and Key Drug Causes