Chapter 2 of 5 - Endocrine System Course

Hypothalamus & Pituitary Gland

The hypothalamus and pituitary gland form the central command unit of the endocrine system - translating neural signals into hormonal responses that regulate growth, metabolism, reproduction, and stress.

The Hypothalamus - Bridge Between Brain and Hormones

The hypothalamus is a small region at the base of the diencephalon, sitting just below the thalamus and above the pituitary gland. Despite weighing only about 4 grams, it serves as the primary link between the nervous system and the endocrine system. It receives input from virtually every part of the brain - including the limbic system, cerebral cortex, and brainstem - and converts these neural signals into hormonal outputs.

The hypothalamus controls the pituitary gland through two distinct mechanisms:

  • Hypophyseal portal system - a specialized capillary network that carries releasing and inhibiting hormones from the hypothalamus directly to the anterior pituitary
  • Hypothalamo-hypophyseal tract - axons of hypothalamic neurons that extend down into the posterior pituitary, where hormones are stored and released

Beyond endocrine control, the hypothalamus also regulates body temperature, hunger and satiety, thirst, circadian rhythms, and autonomic nervous system function - making it one of the most functionally diverse structures in the brain.

Hypothalamic Releasing and Inhibiting Hormones

The hypothalamus produces several small peptide hormones (and one amine) that travel through the hypophyseal portal system to reach the anterior pituitary. These hormones either stimulate (releasing) or suppress (inhibiting) secretion of specific anterior pituitary hormones.

Hypothalamic HormoneAbbreviationAction on Anterior Pituitary
Gonadotropin-releasing hormoneGnRHStimulates release of FSH and LH
Thyrotropin-releasing hormoneTRHStimulates release of TSH (and prolactin)
Corticotropin-releasing hormoneCRHStimulates release of ACTH
Growth hormone-releasing hormoneGHRHStimulates release of GH
Somatostatin (GHIH)SS / GHIHInhibits release of GH (and TSH)
Dopamine (PIH)DA / PIHInhibits release of prolactin

A key clinical point: dopamine is the primary inhibitor of prolactin. If the pituitary stalk is severed (cutting off dopamine delivery), prolactin levels rise - unlike every other anterior pituitary hormone, which would fall without hypothalamic input. This is why prolactin is the only anterior pituitary hormone under predominantly inhibitory control.

Quick Check

Which hypothalamic hormone primarily inhibits prolactin secretion from the anterior pituitary?

Anterior Pituitary (Adenohypophysis)

The anterior pituitary originates from Rathke's pouch - an ectodermal outgrowth of the oral cavity (pharyngeal epithelium). It is a true glandular structure that synthesizes, stores, and secretes its own hormones. It accounts for about 80% of the pituitary gland by weight and produces six major hormones.

A helpful mnemonic for the anterior pituitary hormones: "FLAT PiG" - FSH, LH, ACTH, TSH, Prolactin, GH.

HormoneCell TypeTargetPrimary Action
Growth Hormone (GH)SomatotrophsLiver, bone, musclePromotes growth via IGF-1; increases blood glucose
TSHThyrotrophsThyroid glandStimulates thyroid hormone synthesis (T3/T4)
ACTHCorticotrophsAdrenal cortexStimulates cortisol secretion (zona fasciculata)
FSHGonadotrophsOvaries / testesFollicle development (F) / spermatogenesis (M)
LHGonadotrophsOvaries / testesOvulation and progesterone (F) / testosterone (M)
ProlactinLactotrophsMammary glandsStimulates milk production; inhibits GnRH

Note that somatotrophs make up roughly 50% of the cells in the anterior pituitary - making GH the most abundantly produced anterior pituitary hormone. This is clinically relevant because pituitary adenomas most commonly arise from somatotrophs (GH-secreting) or lactotrophs (prolactin-secreting).

Fill in the Blank

The anterior pituitary develops from________- an ectodermal outgrowth of the oral cavity, while the posterior pituitary develops from neural ectoderm (a downward extension of the brain).

Posterior Pituitary (Neurohypophysis)

The posterior pituitary is not a true gland - it is a downward extension of neural tissue from the hypothalamus. It does not synthesize any hormones. Instead, it stores and releases two hormones that are produced by neurosecretory cells in the hypothalamus:

Hypothalamus

Supraoptic nucleus produces ADH - Paraventricular nucleus produces oxytocin

Hypothalamo-hypophyseal tract

Axons transport hormones down to posterior pituitary

Posterior Pituitary (storage and release)

Hormones stored in axon terminals - released into blood on neural signal

HormoneSource NucleusTargetPrimary Action
ADH (vasopressin)Supraoptic nucleusKidneys (collecting ducts)Increases water reabsorption - concentrates urine
OxytocinParaventricular nucleusUterus, mammary glandsUterine contractions (labor) and milk letdown reflex

ADH acts on V2 receptors in the collecting ducts of the kidney to insert aquaporin-2 channels, allowing water to be reabsorbed from the filtrate. At higher concentrations, ADH also acts on V1 receptors in vascular smooth muscle to cause vasoconstriction - hence the alternative name "vasopressin."

Oxytocin operates through a positive feedback mechanism during childbirth - uterine contractions push the baby against the cervix, which triggers more oxytocin release, which triggers stronger contractions, and so on until delivery.

Quick Check

A patient has lost the ability to concentrate urine and is producing large volumes of very dilute urine. Which hormone deficiency is most likely responsible?

Hypothalamic-Pituitary Axes - Feedback Loops

The hypothalamus and pituitary communicate with peripheral endocrine glands through tightly regulated negative feedback loops. When the end-organ hormone rises to a sufficient level, it feeds back to suppress both the hypothalamus and the pituitary, reducing further stimulation. Three major axes govern this communication:

HPA Axis

Hypothalamus

CRH

Anterior Pituitary

ACTH

Adrenal Cortex

Cortisol

Cortisol feeds back (-)

HPT Axis

Hypothalamus

TRH

Anterior Pituitary

TSH

Thyroid Gland

T3 / T4

T3/T4 feeds back (-)

HPG Axis

Hypothalamus

GnRH

Anterior Pituitary

FSH / LH

Gonads

Estrogen / Testosterone

Sex steroids feed back (-)

Understanding these axes is critical for interpreting lab values. For example, a patient with high cortisol and low ACTH likely has a primary adrenal tumor (the cortisol is suppressing ACTH via negative feedback). Conversely, high cortisol and high ACTH suggests an ACTH-secreting pituitary adenoma (Cushing disease), where the tumor escapes normal feedback control.

Fill in the Blank

In the HPA axis, the hypothalamus secretes CRH, which stimulates the anterior pituitary to release ACTH, which in turn stimulates the adrenal cortex to produce________- a glucocorticoid that then feeds back to suppress both CRH and ACTH.

Clinical Correlations

Disorders of the hypothalamic-pituitary system often result from either excess or deficiency of specific hormones. Understanding the normal physiology makes these conditions straightforward to predict.

Acromegaly & Gigantism (GH Excess)

Excess growth hormone in children (before epiphyseal plate closure) causes gigantism - proportional overgrowth of the entire skeleton. In adults (after plate closure), it causes acromegaly - enlargement of the hands, feet, jaw (prognathism), and soft tissues. Most cases result from a GH-secreting pituitary adenoma. Diagnosis involves measuring serum IGF-1 and performing an oral glucose tolerance test (GH should normally be suppressed by glucose but is not in acromegaly).

Pituitary Dwarfism (GH Deficiency)

Deficiency of growth hormone in childhood leads to proportional short stature - the child has normal body proportions but is significantly shorter than expected. Unlike achondroplasia (a genetic skeletal dysplasia causing disproportionate dwarfism), pituitary dwarfism can be treated with exogenous recombinant GH (somatropin) if diagnosed early.

SIADH (Syndrome of Inappropriate ADH Secretion)

Excessive ADH secretion - often caused by small cell lung cancer, CNS disorders, or certain drugs - leads to excessive water retention, dilutional hyponatremia (low serum sodium), concentrated urine, and decreased serum osmolality. Treatment involves fluid restriction and, in severe cases, vasopressin receptor antagonists (vaptans) or hypertonic saline.

Diabetes Insipidus (ADH Deficiency or Resistance)

Central diabetes insipidus results from inadequate ADH production (hypothalamic/pituitary damage), while nephrogenic diabetes insipidus results from kidney resistance to ADH (often from lithium use or genetic mutations in V2 receptors). Both produce massive volumes of dilute urine (up to 20 L/day), severe thirst, and hypernatremia. Central DI responds to desmopressin (synthetic ADH) - nephrogenic DI does not.

Sheehan Syndrome (Postpartum Pituitary Necrosis)

During pregnancy, the pituitary gland enlarges significantly (primarily due to lactotroph hyperplasia) but its blood supply does not increase proportionally. If the mother experiences severe postpartum hemorrhage and hypotension, the enlarged pituitary can undergo ischemic necrosis. The result is panhypopituitarism - deficiency of all anterior pituitary hormones. The earliest sign is often failure to lactate (loss of prolactin), followed by fatigue, amenorrhea, and signs of hypothyroidism and adrenal insufficiency.

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