Sheehan syndrome

Mechanisms and manifestations of adenohypophyseal hypofunction

In addition to isolated Sheehan syndrome, decreased activity of the anterior pituitary gland (hypopituitarism) can occur with a deficiency of one, several, or even all tropic hormones simultaneously. If the pathology is caused by a space-occupying lesion (tumor), the patient develops characteristic manifestations of the so-called mass effect:

• Enlargement of the sella turcica.
• Compression of the optic chiasm and nerves, leading to visual field defects (bitemporal hemianopsia).
• Signs of increased intracranial pressure accompanied by persistent headaches, nausea, and vomiting.

Another striking example of hypofunction, but affecting the somatotropic axis, is growth hormone (GH) deficiency. If this condition occurs in childhood, it provokes the development of pituitary dwarfism. These patients are characterized by a strictly proportional delay in physical growth with completely preserved intellectual development.

Opposite conditions: classification of hyperpituitarism

In addition to hypofunction, excessive production of adenohypophyseal hormones is frequently encountered in clinical practice. The classification of hyperpituitarism includes the following main forms:

1. Pituitary gigantism.
2. Acromegaly.
3. Hyperprolactinemia.
4. Hypermelanotropinemia.
5. Pituitary precocious puberty syndrome (true).
6. Pituitary hyperthyroidism.
7. Pituitary hypercorticism (known as Cushing's disease).

Pathologies of the somatotropic axis in hyperfunction

Excessive secretion of somatotropin leads to two different diseases depending on the age of manifestation:

Pituitary gigantism occurs in childhood or adolescence when ossification of the epiphyseal growth plates is not yet complete. It can occur in a primary glandular type (when acidophilic pituitary cells synthesize too much GH) or a post-glandular receptor type (when target tissues have an abnormally high affinity for the hormone).

Acromegaly develops in adults whose growth plates are already closed. This disease manifests as enlargement of the hands, feet, and facial features (enlarged nose, brow ridges, protruding lower jaw — prognathism, widened spaces between teeth). Soft tissues also thicken, the voice becomes coarser, and internal organs enlarge (splanchnomegaly). Due to the powerful counter-insulin action of GH, patients often develop somatotropic (steroid) diabetes mellitus. In the psycho-emotional sphere, drowsiness, general sluggishness, and mild euphoria are observed, sometimes alternating with bouts of anger or tearfulness.

Excessive activity of the lactotropic axis

The absolute opposite of prolactin deficiency (as in Sheehan syndrome) is hyperprolactinemia. Excessive production of this hormone leads to infertility, various menstrual cycle disorders (ranging from mild hypomenorrhea to complete amenorrhea), and galactorrhea. Notably, galactorrhea can occur even with normal blood prolactin levels if the mammary gland receptors have an increased sensitivity to it.

In the so-called asymptomatic form, the level of the biologically active hormone is high, but about half of the patients complain only of dizziness, headaches, and short-term blood pressure spikes. Anovulation and impaired follicular maturation are recorded in the ovaries. The psyche also undergoes changes: an excessive need to care for others, especially children, appears.

For accurate diagnosis of the pathology, anamnesis is collected, a gynecological examination is performed, and the function of the adrenal cortex and thyroid gland is checked. Excess prolactin is detected in the blood, and the balance of sex hormones is evaluated. Functional tests using dopamine agonists (e.g., bromocriptine) and its antagonists (metoclopramide) play an important role.

Disorders of the pro-opiomelanocortin (POMC) axis

Pathologies of this group include hypermelanotropinemia and Cushing's disease. They are caused by hypersecretion of ACTH and other related peptides of the POMC family. Excess ACTH and melanocyte-stimulating hormone causes pronounced skin hyperpigmentation ("bronze diabetes"), which also occurs in primary adrenal insufficiency due to feedback mechanism failure.

Cushing's disease is characterized by specific centripetal (dysplastic) obesity with the formation of a "buffalo hump" and a moon face (matronism). Broad purple striae appear on the skin, muscle weakness, arterial hypertension, and steroid diabetes develop. Patients experience decreased libido and menstrual irregularities.

Class and exam questions

What else to study on this topic

• Mechanisms of development of steroid (somatotropic) diabetes mellitus in acromegaly and Cushing's disease
• Functional tests with bromocriptine and metoclopramide for the diagnosis of hyperprolactinemia
• Pathogenesis of primary glandular and receptor variants of pituitary gigantism
• Mechanism of feedback disinhibition in primary adrenal insufficiency

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.