USMLE Step 1 video lessons
Foundational science for USMLE Step 1: the mechanisms behind the numbers, drawn step by step, each lesson ending with an original exam-style question.
Cardiac physiology, the pressure-volume loop, haemodynamics and the heart in disease.
Cardiovascular physiology · series of 16
5:00Pressure-volume loop explained: four phases, four valve events
One heartbeat drawn as a single shape. Learn which corner of the pressure-volume loop is which valve, which way the loop runs, and how to read stroke volume and ejection fraction straight off it.
5:04Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR
Give fluid or lose blood, and the same heart draws a different loop. See how preload slides one corner of the pressure-volume loop, and why the other side barely moves.
4:49Afterload on the pressure-volume loop
Afterload on the pressure-volume loop is a line, not a number. Pivot it and the end-systolic point slides along a fixed ESPVR: higher afterload means a taller, narrower loop and less blood out.
5:17Contractility on the pressure-volume loop: the ESPVR explained
Contractility on the pressure-volume loop shows up as the slope of the ESPVR. More contractility steepens it, so ejection runs to a smaller volume; less contractility flattens it.
Heart sounds, murmurs and ECG · series of 6
5:26S2 splitting and heart sounds S1–S4, explained
Heart sounds are valves closing. Read S2 splitting with two questions: which valve is late, and does the gap move with breathing?
5:15Heart murmurs and dynamic manoeuvres, from preload and afterload
A murmur follows the flow: manoeuvres that change preload or afterload change how much blood crosses the lesion. Hypertrophic obstructive cardiomyopathy is the exception that flips the rule.
5:31HOCM vs aortic stenosis murmur: telling them apart at the bedside
Both murmurs are harsh and systolic. The difference is the obstruction: a fixed valve in aortic stenosis, a dynamic muscle and mitral leaflet in HOCM. The manoeuvres follow from that.
5:15Ventricular action potential: phases 0 to 4 and their ion currents
A ventricular muscle cell takes about a quarter of a second to fire. Match each phase to its ion current, then to the antiarrhythmic class that acts on it.
The kidney from filtration and clearance to acid-base balance, electrolytes and tubular disorders.
Renal & acid–base · series of 21
5:35ABG interpretation, made simple
ABG interpretation from three numbers: pH, PaCO₂ and HCO₃⁻. Learn the normal ranges, the 20 : 1 ratio behind pH, and a three-step method for naming the primary disorder and its compensation.
5:25Anion gap explained: high vs normal gap metabolic acidosis
How to calculate the anion gap, why an added acid widens it while bicarbonate loss does not, and how a low albumin can hide a high-gap acidosis.
5:10Winters' formula: the expected PaCO₂ in metabolic acidosis
Winters' formula tells you how far the PaCO₂ should fall in a metabolic acidosis. Compare the measured value with that window and a hidden respiratory disorder shows itself.
5:09Delta ratio: find the hidden second acid–base disorder
The delta ratio compares the rise in the anion gap with the fall in bicarbonate. In a high anion gap acidosis, it shows whether a second metabolic disorder is hiding.
Renal physiology · series of 8
5:25GFR and Starling forces at the glomerulus
Three pressures across the capillary wall set the net filtration pressure, and GFR is Kf times that number. Use them to predict why a kidney stone lowers filtration.
5:16Afferent vs efferent arteriole: GFR, RPF and filtration fraction
Two resistors set the pressure in the glomerulus. Learn the 2×2 table of afferent and efferent constriction and dilation, and use it to explain NSAID and ACE inhibitor kidney injury.
5:20Renal clearance: inulin, creatinine and PAH
Renal clearance is a bookkeeping volume, not a real flow. Use the same equation to estimate GFR with inulin and creatinine, effective renal plasma flow with PAH, and to read what the tubule did.
4:55Glucose transport maximum, splay and SGLT2
Glucosuria is not a leak in a healthy pipe. It appears when the filtered load exceeds a finite carrier capacity, the glucose transport maximum, and splay makes it start earlier than the simple threshold predicts.
Lung mechanics, gas exchange, ventilation-perfusion matching and respiratory disease.
Respiratory physiology · series of 10
5:26Lung volumes and capacities, explained
Every lung volume and capacity on a spirogram, and why residual volume, FRC and total lung capacity need more than spirometry.
5:23Obstructive vs restrictive lung disease: FEV1/FVC and loops
How the FEV1/FVC ratio, total lung capacity and the shape of the flow-volume loop separate obstructive from restrictive lung disease in a patient who is short of breath.
5:23Lung compliance, Laplace and surfactant: why alveoli stay open
A film of water lines every alveolus and pulls inward on it. Lung compliance, the law of Laplace and surfactant explain why the lungs do not collapse at the end of each breath.
5:18V/Q mismatch: shunt, dead space and the oxygen test
Shunt, dead space and low V/Q all mismatch ventilation and perfusion, yet only shunt barely responds to oxygen. The oxygen test sorts the three.
Digestion, absorption, hepatobiliary physiology and gastrointestinal disease.
GI physiology and pathology · series of 4
5:14GI hormones: gastrin, CCK, secretin, GIP and motilin
Each gut hormone answers one question: what has just arrived, and what must the gut do about it? Match every hormone to its source cell, its stimulus and its actions.
4:52Gastric acid secretion: the parietal cell, step by step
Three signals converge on one proton pump, and acid also brakes its own release. Follow the parietal cell, then see where PPIs, H₂ blockers and somatostatin act.
5:14H. pylori and peptic ulcer disease: how mucosal defence fails
More than a third of people worldwide carry H. pylori, yet only a minority develop an ulcer. This lesson builds the balance between acid and mucosal defence, then shows how H. pylori and NSAIDs break it.
5:44Bilirubin metabolism and jaundice: pre-hepatic, hepatic, post-hepatic
Jaundice is one sign with three places to fail. Follow bilirubin from haem to the gut, then use the fraction, the enzymes, the urine and the stool to find where the pathway breaks.
Hormone axes, feedback loops and the endocrine disorders that follow when they fail.
Endocrinology · series of 14
5:05Hypothalamic-pituitary axes and feedback: primary, secondary, tertiary
Every hypothalamic-pituitary axis is a three-step chain held in check by negative feedback. Use that logic to predict which hormones rise or fall when the fault is in the gland, the pituitary or the hypothalamus.
5:13Primary vs secondary endocrine disorders: paired hormone levels
Two numbers, read together, tell you whether the gland or the pituitary is failing. Learn the two-number rule for primary vs secondary endocrine disorders across the adrenal, thyroid and gonadal axes.
5:06Insulin secretion in the beta cell: from glucose to granule
A beta cell has no eyes and no taste buds, yet it answers a rise in glucose within minutes. Follow the six steps, and see where sulfonylureas and diazoxide act on the KATP channel.
5:19Insulin vs glucagon signalling: receptors and effects
Insulin vs glucagon: two islet hormones, two receptor families, and three target tissues. Why a glucagon injection rescues hypoglycaemia through the liver, not muscle.
Neuroscience, special senses, behavioural science and psychiatry.
Neuroanatomy and lesion localisation · series of 16
5:08Upper vs lower motor neuron lesions: signs and localisation
Weak is weak, but the muscle tells you which neuron broke. Learn the signs of upper and lower motor neuron lesions and use them to place the damage.
5:01Dorsal column vs spinothalamic tract: where each pathway crosses
Both sensory pathways start in the same ganglion and end in the same cortex, but one crosses in the medulla and the other in the cord. That one fact predicts the pattern of sensory loss.
5:06Spinal cord syndromes compared: rebuild each from three tracts
Every spinal cord syndrome is the same cross-section with a different shape of damage. Three tracts and the cord's blood supply are enough to predict each pattern.
5:10Cranial nerve nuclei: a brainstem map by level and position
Ten pairs of cranial nerves have nuclei in the brainstem, and they look like a list to memorise. Two rules sort them, level and position from the midline, with one exception: the trigeminal nuclei run the whole length.
Blood, haemostasis, anaemia, haematological malignancy and tumour biology.
Haematology and oncology · series of 14
5:37Microcytic anaemia: four causes, four iron fingerprints
In microcytic anaemia, small red cells look alike under the microscope, but each cause breaks a different step of haemoglobin making. The iron studies, the red cell count and HbA₂ show which step failed.
5:34Hepcidin: why iron falls in inflammation
Hepcidin is the liver hormone that locks iron inside cells. It explains why serum iron drops in inflammation without any bleeding, and how ferritin and iron-binding capacity tell it apart from iron deficiency.
5:23B12 vs folate deficiency: MMA, homocysteine and the nerves
How to tell B12 deficiency from folate deficiency using methylmalonic acid, homocysteine and the nervous system, and why folic acid alone can fix the blood while the nerves worsen.
5:27Intravascular vs extravascular haemolysis: site and labs
Both kinds of haemolysis destroy red cells too early. The site of destruction, and what haptoglobin, LDH, bilirubin and urine show, tells them apart.
Innate and adaptive immunity, hypersensitivity, immunodeficiency and transplantation.
Immunology · series of 14
5:03MHC I vs MHC II: how antigen presentation works
MHC I vs MHC II comes down to one rule: class I shows what the cell made inside, class II shows what the cell swallowed from outside. Each class has its own machinery and its own T cell.
4:58T-cell activation: the two-signal model
A T cell can recognise its antigen perfectly and still stay asleep. T-cell activation needs a second signal, and the antigen-presenting cell decides whether it is given.
5:13Th1, Th2, Th17 and Treg: helper T-cell subsets
Th1, Th2, Th17 and Treg are chosen by the cytokines around a naive CD4 T cell. Each has an inducer, a master transcription factor, a product and a target.
5:13Antibody isotypes and class switching
Every antibody class has one main job. A B cell can change its class without changing what it recognises, and the helper T cell and the enzyme AID decide how.
How drugs act and move through the body: dose-response, pharmacokinetics, autonomic drugs and antimicrobial mechanisms.
Pharmacology: principles and autonomic drugs · series of 16
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.
All 16 lessons in Pharmacology: principles and autonomic drugs
Bacterial structure, toxins and genetics, antibiotic resistance, viruses, fungi and the organisms behind classic infections.
Microbiology · series of 14
5:39Gram-positive vs gram-negative cell walls
The Gram stain looks like a dye test, but it is a wall test. Compare the two cell envelopes and use them to predict the stain and antibiotic susceptibility.
5:01Acid-fast stain and the mycobacterial cell wall
Mycobacteria wrap their wall in wax. That one feature explains why the acid-fast stain works, why Gram staining does not, and why many antibiotics struggle to get in.
5:46Endotoxin vs exotoxin: lipid A, A-B toxins and toxoids
Endotoxin is a piece of the gram-negative outer membrane. An exotoxin is a protein that living bacteria secrete. Both can cause shock, but they differ in source, chemistry, mechanism and effect.
5:54Bacterial toxins that raise cAMP: cholera, pertussis, anthrax
Four toxins from four bacteria all push cyclic AMP up, but each takes a different route. Knowing the route, and the cell it acts on, predicts the clinical picture.