Endocrine Physiology EN

Hormones act through receptors whose location and signalling depend on hormone chemistry. Endocrine axes commonly use hierarchical control and negative feedback.

Map hypothalamus/pituitary/target gland when relevant, then identify feedback signal and target.

Endocrine testing often relies on understanding feedback rather than interpreting one concentration in isolation.

A hormone concentration can be inappropriate even if it lies within a laboratory reference interval, depending on the physiological context.

Pituitary hormones coordinate several target glands; thyroid hormones increase metabolic activity and are essential for normal growth and development. TSH is regulated by hypothalamic input and thyroid-hormone feedback.

Use axis logic: controller → trophic hormone → target hormone → feedback.

Primary versus central thyroid disorders can often be distinguished by the relationship between TSH and thyroid hormones.

TSH should not be interpreted independently of thyroid hormone when evaluating an axis.

Adrenal cortex produces mineralocorticoids, glucocorticoids and androgens; medulla releases catecholamines. Cortisol supports stress adaptation and metabolism, while aldosterone regulates sodium/potassium balance.

Separate cortisol control through ACTH from aldosterone control dominated by RAAS and potassium.

Adrenal excess or deficiency alters blood pressure, electrolytes, glucose and stress tolerance.

All adrenal hormones are not controlled by the same upstream signal.

Insulin promotes nutrient storage and lowers circulating glucose by coordinated effects on liver, muscle and adipose tissue; glucagon supports glucose availability during fasting.

Think fed state versus fasting state and tissue-specific actions.

Diabetes reflects inadequate effective insulin action and causes metabolic consequences beyond glucose alone.

Insulin does more than move glucose into cells; it coordinates carbohydrate, fat and protein metabolism.

Endocrine glands release hormones into the circulation so they can influence distant targets. Hormone effect depends on concentration, receptor availability, receptor affinity, downstream signalling and target-cell context. Peptide and catecholamine hormones generally use membrane receptors, whereas steroid and thyroid hormones can act through intracellular receptors and transcriptional mechanisms.

Many endocrine systems are arranged as axes. A hypothalamic signal controls a pituitary trophic hormone, which controls a peripheral gland; the peripheral hormone then feeds back on upstream centres. This organization allows amplification and coordinated regulation.

Clinical reasoning: a hormone value must be interpreted in relation to its controller. Low target-gland hormone with high trophic hormone suggests a different defect from low target hormone with an inappropriately low trophic signal.

Teach it back: construct a generic endocrine axis and show how primary target-gland failure changes both downstream and upstream hormone concentrations.

Hypothalamic TRH supports pituitary TSH secretion, and TSH stimulates thyroid hormone synthesis and release. Circulating thyroid hormones feed back to reduce upstream drive. Thyroid hormones influence basal metabolic activity, cardiovascular function, thermogenesis and normal growth and nervous-system development.

Because of negative feedback, primary thyroid failure tends to reduce circulating thyroid hormone while increasing TSH if pituitary function is intact. Central failure can produce low thyroid hormone without the expected TSH rise.

Clinical reasoning: interpretation therefore requires paired thinking rather than labelling TSH or thyroid hormone independently.

Teach it back: explain why a high TSH can be an appropriate physiological response to a failing thyroid gland.

The adrenal cortex produces mineralocorticoids, glucocorticoids and adrenal androgens. Cortisol secretion is strongly linked to the hypothalamic-pituitary-adrenal axis and has broad metabolic and permissive effects during stress. Aldosterone is regulated importantly by angiotensin II and extracellular potassium, allowing sodium conservation and potassium excretion to respond to circulatory and electrolyte needs.

The adrenal medulla releases catecholamines during sympathetic activation, supporting rapid cardiovascular and metabolic responses. Thus “adrenal hormone” is not one regulatory category; different zones serve different control systems.

Clinical reasoning: adrenal deficiency or excess can disturb blood pressure, glucose, electrolytes and the ability to tolerate physiological stress.

Teach it back: explain why low effective circulating volume strongly stimulates aldosterone even though ACTH is not its dominant physiological controller.

After a meal, rising nutrient availability promotes insulin secretion. Insulin favours glucose uptake in responsive tissues, glycogen formation, lipid storage and protein anabolism while restraining excessive hepatic glucose output and lipolysis. During fasting, lower insulin and relatively greater glucagon action support hepatic glucose production and mobilization of stored fuel.

The key idea is coordinated whole-body fuel partitioning, not simply “insulin lowers glucose.” Severe loss of effective insulin action shifts metabolism toward increased hepatic glucose production, lipolysis and ketone generation while reducing appropriate anabolic storage.

Clinical reasoning: diabetes therefore affects carbohydrate, fat, protein, fluid and electrolyte physiology, not glucose alone.

Teach it back: compare the fed and fasting states using insulin, glucagon, liver, skeletal muscle and adipose tissue.