Pharmacology: USMLE Step 1 video lessons
How drugs act and move through the body: dose-response, pharmacokinetics, autonomic drugs and antimicrobial mechanisms.
Dose-response and antagonism, the therapeutic index, bioavailability, volume of distribution, clearance and half-life, elimination kinetics, dosing calculations, CYP450 interactions, autonomic receptors, beta blockers, pressors, cholinergic toxicity and the antibiotic mechanisms that bridge into microbiology.
5:17Potency vs efficacy: EC50, Emax and agonist types
Potency vs efficacy: potency is where a dose-response curve sits, efficacy is how high it reaches. Learn to read EC50 and Emax, and to tell full, partial and inverse agonists apart.
5:01Competitive vs noncompetitive antagonists: effect on EC50 and Emax
Two antagonists can block the same receptor, yet only one can be beaten by more agonist. The shape of the dose-response curve tells them apart.
5:01Therapeutic index explained: TD50 / ED50
Two drugs can be equally potent and very different in safety. The therapeutic index compares the toxic dose with the effective dose, and explains why some drugs need monitoring.
5:18First-pass metabolism and bioavailability: calculating oral F from AUC
A swallowed drug passes through the gut wall and liver before it reaches the circulation. Learn how first-pass metabolism lowers bioavailability and how to calculate oral F from AUC and dose.
5:17Volume of distribution: why Vd can be bigger than the body
Volume of distribution is the amount of drug in the body divided by the plasma concentration. It is an apparent volume, so it can be far larger than the body itself.
5:01Clearance and half-life: t½ = 0.693 × Vd / CL
How clearance and volume of distribution together set a drug's half-life, and why the half-life is the clock for reaching steady state and for washout.
5:12Zero-order vs first-order elimination explained
First-order elimination removes a constant fraction per unit time; zero-order removes a constant amount. Saturation of metabolizing enzymes turns one into the other.
5:02Loading dose and maintenance dose, explained
A drug with a long half-life takes days to reach target on its own. The loading dose fills the volume of distribution; the maintenance dose replaces what clearance removes.
5:16CYP450 inducers and inhibitors: how they change drug levels
A drug's dose can stay the same while its level changes. Cytochrome P450 inducers and inhibitors turn the clearance dial, and the level, and the effect, follow.
5:33Autonomic receptors: alpha, beta and muscarinic
The same transmitter can do opposite things in different organs, because the receptor and its G protein decide the response. Learn the code and the tissue list once, and the effects follow.
5:24Beta blocker selectivity: beta-1, ISA and alpha blockade
Every beta blocker slows the heart, yet side effects differ. Three questions, selectivity, intrinsic sympathomimetic activity and alpha-1 blockade, predict what each drug does.
5:46Vasopressors compared: receptors, pressure and heart rate
Four adrenergic drugs, four different effects on mean arterial pressure and heart rate. Work them out from the receptors and the baroreflex instead of memorising them.
5:36Organophosphate poisoning: muscarinic vs nicotinic signs
One poison, two halves of the picture, two antidotes. Learn the muscarinic and nicotinic features of organophosphate poisoning and how atropine and pralidoxime work.
5:01Receptor desensitization, downregulation and upregulation
Receptors are regulated, not fixed. Learn why a drug can work less with repeated use, why chronic blockade builds extra receptors, and why beta-blockers are tapered.
5:04Beta-lactams and vancomycin: enzyme versus substrate
Beta-lactams and vancomycin both stop the bacterial cell wall being built, but one grips the enzyme and the other grips the substrate. That single difference explains their reach and their resistance patterns.
5:07Protein synthesis inhibitors: 30S vs 50S antibiotics
Sort protein synthesis inhibitors by ribosomal subunit and the step they block, then link each class to its signature adverse effect.