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Let's talk about hypothalamic and pituitary hormone deficiency. In the anterior pituitary gland,
deficiencies of ACTH manifest a secondary cortisol deficiency. Thyroid stimulating hormone
manifests central hypothyroidism and this is covered in the thyroid section. Gonadotropin
deficiency can manifest with amenorrhea. Growth hormone deficiency in individual's prepuberty
manifests with prolactin hormone deficiency. In the posterior pituitary gland, oxytocin may be
decreased and antidiuretic hormone may be decreased resulting in central diabetes insipidus
versus peripheral diabetes insipidus. There are a number of pituitary hormone deficiency
states; hypopituitarism, pituitary apoplexy, and growth hormone deficiency. The causes of
hypopituitarism include pituitary adenomas, pituitary surgery, pituitary radiation, apoplexy or
infarction. Craniopharyngiomas, metastatic tumors, even meningiomas can cause compression
of the pituitary. Lymphocytic hypophysitis and sarcoidosis are much rarer manifestations as
of the conditions listed here. One or more pituitary hormone deficiencies is usually the
definition of hypopituitarism. Growth hormone, FSH, LH are the most sensitive hormones to
injury and the most commonly deficient. Panhypopituitarism, on the other hand, is the situation
where the patient lacks all of the anterior pituitary hormones. This is usually due to a very
large tumor or pituitary surgery. There is a need to replace thyroxin and cortisol in the setting.
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Replacement of 6 steroids and growth hormone depend on the age of the patient and the
clinical benefits. Secondary cortisol deficiency is commonly iatrogenic due to exogenous
glucocorticoid suppression of pituitary ACTH secretion. Patients with secondary cortisol deficiency
have only glucocorticoid deficiency and the rest of the adrenal gland functions normally as
does the renin angiotensin system. They're at less risk for hypotension and hyponatremia
and adrenal crisis than those with primary cortisol deficiency because the production of
mineralocorticoid is retained. Unlike patients with primary cortisol deficiency, patients with
secondary cortisol deficiency do not develop hyperpigmentation or bronzing of the skin. This is
because ACTH and its prohormone which is responsible for these changes, proopiomelanocortin
or POMC is not hypersecreted. TSH deficiency leads to secondary or central hypothyroidism.
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Secondary hypothyroidism is clinically identical to primary hypothyroidism. Thyroid-stimulating
hormone deficiency can be diagnosed by demonstrating a simultaneously inappropriately
normal or low TSH level with a low T4 either free or total. The treatment involves levothyroxine
replacement for primary hypothyroidism. Serum TSH cannot be used to monitor and assess
for adequacy of thyroid hormone replacement. Levothyroxine dose is adjusted based on free
T4 levels with a goal of obtaining a value within the normal reference range. Growth hormone
deficiency prior to puberty will lead to short stature. In adulthood, growth hormone production
is not as important for growth as during childhood. In adults, growth hormone deficiency
causes fatigue, loss of muscle mass, and increase in the ratio of fatty tissue to lean tissue
and increased risk for osteoporosis. Evaluation for growth hormone deficiency is
recommended in patients with at least 1 known pituitary hormone deficiency. Unfortunately,
growth hormone therapy has been used inappropriately as an alternative medication without
good evidence to support its use. Let's talk about gonadotropin-releasing hormone deficiency.
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The pituitary gland normally secretes LH and FSH in response to GNRH from the hypothalamus.
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Luteinizing hormone and follicle stimulating hormone stimulates the secretion of normal male
and female sex hormones. LH and FSH deficiency causes hypogonadotropic hypogonadism.
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Causes include hypothalamic amenorrhea in women associated with excess exercise as seen in
professional athletes or severe illness or anorexia. Congenital GnRH deficiency is seen in
Kallmann syndrome. This condition occurs when hypothalamic neurons responsible for releasing
GnRH fail to migrate into the hypothalamus during embryonic development. The treatment, if
fertility is the goal, replace gonadotropins in men and women. In women who are
premenopausal who do not desire fertility, estrogen and progesterone containing oral
contraceptives should be provided. Treatment also is recommended to avoid loss of estrogen
dependent bone at a young age which could lead to osteoporosis. Postmenopausally,
hypogonadotropic hypogonadism treatment is not indicated. In men, if fertility is not desired
testosterone replacement therapy can be offered.