Acute Hypopituitarism: Overview, Diagnostic Considerations …

Posted: May 29, 2019 at 8:50 pm

Adrenocorticotropic hormone deficiency

A deficiency of adrenocorticotropic hormone (ACTH), or corticotropin, is characterized by a decrease in adrenal androgens and production of cortisol. Acute loss of adrenal function is a medical emergency and may lead to hypotension and death if not treated.

Signs and symptoms of ACTH deficiency may be profound and potentially fatal; they include myalgias, arthralgias, fatigue, headache, weight loss, anorexia, nausea, vomiting, abdominal pain, altered mentation or altered consciousness, dry wrinkled skin, decreased axillary and pubic hair, anemia of chronic disease, dilutional hyponatremia, hypoglycemia, hypotension, and shock.

Symptoms are nearly identical to those of primary adrenal insufficiency but can be differentiated by lack of hyperpigmentation. Hyperpigmentation occurs in a long feedback loop in which a cortisol deficiency results in increased production of ACTH by the pituitary. The ACTH precursor coupled to melanocyte-stimulating hormone is not produced in patients with pituitary disease, and therefore, hyperpigmentation does not take place.

Patients with secondary adrenal insufficiency usually are eukalemic. This differs from primary adrenal insufficiency, in which patients develop hyponatremia and hyperkalemia. Aldosterone secretion is not affected, as it does not depend on corticotropin but instead on the renin-angiotensin axis.

Secondary hypothyroidism due to decreased TSH (also known as thyrotropin) exhibits symptoms identical to those of primary thyroid disease, only typically less severe. Signs and symptoms of secondary hypothyroidism include fatigue, weakness, weight gain, thickened subcutaneous tissues, constipation, cold intolerance, altered mental status, impaired memory, and anemia. Physical examination of the patient may reveal bradycardia, delayed relaxation of the deep tendon reflexes, and periorbital edema.

Low levels of the gonadotropins--follicle-stimulating hormone (FSH) and luteinizing hormone (LH) --increase the risk of osteoporosis due to decreased bone density and result in hypogonadism in men and women. In men, symptoms include decreased libido, varying degrees of erectile dysfunction, decreased ejaculate, muscle weakness, and fatigue. Men with long-standing hypogonadism have decreased hair growth, soft testes, and gynecomastia.

Patients may be anemic due to decreased erythropoietin production, which causes a normochromic, normocytic anemia. Pubic and axillary hair growth is usually normal unless a concomitant ACTH deficiency exists.

Premenopausal women present with altered menstrual function, ranging from regular anovulatory periods to amenorrhea, as well as hot flashes, decreased libido, breast atrophy, vaginal dryness, and dyspareunia. Postmenopausal women usually present with headache or visual abnormalities due to other hormonal deficiencies or mass lesions.

In children, FSH and LH deficiency can cause eunuchoidism and lack of sexual development. FSH and LH have an indirect effect on bone growth by causing closure of the epiphysis. Characteristics of eunuchoidism are due to delay in closure of the epiphysis, resulting in long extremities.

In children, growth hormone (GH) deficiency presents as growth retardation and delayed sexual maturation. Patients may present with fasting hypoglycemia due to loss of the gluconeogenic effect of GH, which counteracts the effect of insulin. In adults, GH deficiency presents as weakness, poor wound healing, decreased exercise tolerance, and decreased social functioning.

Tumor growth that decreases prolactin (PRL) production affects the process of lactation; these tumors become evident only in the postpartum state. PRL deficiency is very rare; any process that affects the hypothalamus and the pituitary stalk decreases the normal inhibitory effect of dopamine from the hypothalamus on the pituitary, causing a rebound increase in PRL.

Antidiuretic hormone (ADH) deficiency causes polyuria and polydipsia (diabetes insipidus). When deficient in ADH (also known as vasopressin), the distal tubules of the kidney are unable to absorb water, producing very dilute urine and increasing serum osmolality. If water excretion exceeds oral intake, a patient may become hypotensive and hypovolemic, with hypernatremia and elevated serum osmolality. If fluid intake matches fluid output, serum sodium and osmolality may remain normal.

Central diabetes insipidus is caused by a decrease in ADH secretion, in contrast to nephrogenic diabetes insipidus, in which the kidney is ADH resistant.

Deficiency in oxytocin is characterized by a decrease in milk ejection during lactation. Interestingly, women with known oxytocin deficiency undergo normal labor and delivery despite the lack of hormone. One of the initial clues to the presence of Sheehan syndrome should be the lack of lactation secondary to oxytocin deficiency.

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Acute Hypopituitarism: Overview, Diagnostic Considerations ...

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