Endocrine: USMLE Step 1 video lessons
Hormone axes, feedback loops and the endocrine disorders that follow when they fail.
Hypothalamic-pituitary axes and how to read paired hormone levels, insulin secretion and signalling, DKA and HHS, diabetes drugs, thyroid hormone synthesis, calcium homeostasis, adrenal steroidogenesis and CAH, Cushing syndrome, hyperaldosteronism, SIADH and diabetes insipidus, and the MEN syndromes.
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.
5:58DKA vs HHS pathophysiology: why only one makes acid
Both crises are hyperglycaemic and dehydrated, yet only diabetic ketoacidosis produces acid. The difference is how much insulin is left.
5:58Diabetes drugs by mechanism: where each class acts
Every antidiabetic drug lowers glucose, but each one acts at a different site and carries its own signature side effect. Sort them by mechanism and the side effects follow.
5:14Thyroid hormone synthesis, step by step
Six steps turn iodide into T₄ and T₃, and each antithyroid drug is defined by the step it blocks. Learn the sequence once and the drug map follows.
5:28Calcium homeostasis: PTH, vitamin D and calcitonin
One hormone, PTH, raises calcium yet lowers phosphate. Calcium homeostasis makes sense once you follow PTH, vitamin D and calcitonin across bone, kidney and gut.
5:29Adrenal steroidogenesis: zones, enzymes and the 17α-hydroxylase fork
One gland and one cholesterol pool make three hormone families. Each cortical zone has its own driver and its own enzymes, and 17α-hydroxylase decides which path a steroid takes.
5:44Congenital adrenal hyperplasia: three enzymes, three patterns
Congenital adrenal hyperplasia is one disease family with opposite blood pressures. Ask what piles up, what falls and where it spills to predict the pattern for each enzyme.
5:29Cushing syndrome: the dexamethasone suppression test and ACTH
A normal morning cortisol does not rule out Cushing syndrome. Use screening tests, ACTH and dexamethasone suppression to decide whether the source is the pituitary, an ectopic tumour or the adrenal.
5:27Primary hyperaldosteronism: high aldosterone, low renin
Primary hyperaldosteronism is autonomous aldosterone. Follow it into the collecting duct to explain the hypertension, hypokalaemia, metabolic alkalosis and suppressed renin.
5:44SIADH vs diabetes insipidus: central vs nephrogenic DI
SIADH and diabetes insipidus are both ADH problems that run in opposite directions. Serum sodium, urine osmolality and the response to desmopressin tell them apart.
5:13MEN1, MEN2A and MEN2B: match the gene to its tumours
Two genes explain three syndromes. MEN1 loses a brake (menin); MEN2 jams an accelerator (RET). Once you know the gene, the core tumours follow; the extra features separate MEN2A from MEN2B.