A primary disorder means dysfunction originating in the endocrine gland itself, either hyper- or hypo-function. Examples of a primary dis-order include:
excess cortisol from an adrenal adenoma (Conn’s disease)
decreased thyroid secretion (Hashimoto’s thyroiditis)
reduced ADH secretion (central diabetes insipidus)
A secondary disorder indicates that a disturbance has occurred causing the gland secrete more or less of the hormone. Examples of a secondary disorder include:
Cushing disease (pituitary adenoma secreting ACTH) resulting in hypercortisolism
a dehydrated patient with elevated plasma osmolality causing high ADH levels
Can be caused by autoimmune disease (e.g., type I diabetes, hypothyroidism, primary adrenal insufficiency, gonadal failure), tumors, hemorrhage, infection, damage by neoplasms
Evaluated by a stimulation test
Hypothalamic hormones test anterior pituitary reserve
Injection of the pituitary trophic hormone (e.g., ACTH) tests target gland reserve.
Failure of growth hormone release after arginine injection
Caused by hormone-secreting tumors, hyperplasia, autoimmune stimulation, ectopically produced peptide hormones (e.g., ACTH, ADH)
Evaluated by a suppression test
Failure of glucose to suppress growth hormone diagnostic for acromegaly
Failure of dexamethasone (low dose) to suppress cortisol diagnostic for hypercortisolism
Multiple endocrine neoplasia (MEN) represents a group of inheritable syndromes characterized by multiple benign or malignant tumors.
o MEN 1: hyperparathyroidism, endocrine pancreas, and pituitary adenomas
o MEN 2A: medullary carcinoma of the thyroid, pheochromocytoma, hyperparathyroidism
o MEN 2B: medullary carcinoma of the thyroid, pheochromocytoma, hyperparathyroidism typically absent.
When an endocrine gland does not receive its normal stimulus, it generally undergoes a reversible atrophy.
Long-term high doses of glucocorticoids suppress the ACTH-adrenal axis. Withdrawal of therapy can require up to a year for complete recovery.
Overstimulation of endocrine tissue can cause cell proliferation or hypertrophy in addition to hormone overproduction.
In Graves’ disease, overstimulation of the thyroid tissues causes cell proliferation and this polyclonal expansion creates a goiter in addition to hyperthyroidism.
Tumors, which are generally monoclonal expansions, may also create a hyperfunction. Others produce little if any hormone but are still disease-producing because of the compressive (mass) effect of the additional tissue.
Hypofunction is evaluated by a stimulation test.
Hyperfunction is evaluated by a suppression test.
Lack of glandular stimulation → reversible atrophy.
Overstimulation of a gland → hypertrophy or hyperplasia.