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25 Cards in this Set

  • Front
  • Back
Disorders of the adrenal cortex are related to
hyperfunction or hypofunction.
No known disorders are associated with hypofunction of the adrenal medulla, but medullary hyperfunction causes
clinically defined syndromes.
Hypercortisolism is divided into
ACTH-dependent (Cushing disease or ectopic ACTH syndrome) and ACTH-independent (adrenal adenoma or adenocarcinoma) mechanisms.
Cushing disease is excessive anterior pituitary ACTH production, most commonly by an
ACTH-secreting pituitary microadenoma.
Cushing syndrome occurs whenever there is an excessive level of
cortisol, regardless of cause. Exogenous forms result from exogenous administration of glucocorticoids.
Endogenous forms are either
corticotropin-dependent (most common and caused by an ACTH-secreting pituitary tumor) or corticotropin-independent (usually caused by an adrenal cortical tumor).
Individuals with Cushing disease lose diurnal and circadian patterns of ACTH and cortisol secretion, and they lack the ability to
increase secretion of these hormones in response to a stressor.
Individuals experience
weight gain, glucose intolerance, protein wasting, bone disease, hyperpigmentation, and immunosuppression.
Congenital adrenal hyperplasia is an autosomal recessive disorder with
inadequate synthesis of cortisol and increased levels of ACTH that cause adrenal hyperplasia and overproduction of mineralocorticoids or androgens.
Primary hyperaldosteronism is a disorder of excessive aldosterone secretion usually caused by an
adrenal cortical adenoma or bilateral nodular hyperplasia.
The condition is characterized by
hypertension, hypokalemia, renal potassium wasting, and neuromuscular manifestations.
Secondary hyperaldosterone secretion is related to a variety of conditions associated with
elevated renin release and activation of angiotensin II.
These include decreased circulating blood volume, decreased renal blood supply, (list 3 more)
elevated estrogen levels, Bartter syndrome, and renin-secreting tumors.
Adrenal tumors, adenomas or carcinomas, can autonomously secrete
androgens or estrogens.
Hypofunction of the adrenal cortex can affect
glucocorticoid or mineralocorticoid secretion or both.
Hypofunction can be caused by a deficiency of ACTH or by a
primary deficiency in the gland itself.
Hypocortisolism (low levels of cortisol) is caused by inad¬equate adrenal stimulation by ACTH or by
primary corti¬sol hyposecretion.
Primary adrenal insufficiency is termed
Addison disease.
Addison disease is characterized by
elevated ACTH levels, with inadequate corticosteroid synthesis and output.
Causes include idiopathic autoimmune disease, tuberculosis of the adrenal gland, familial adrenal insufficiency, (list 3 more)
amyloidosis, metastatic destruction of the adrenal glands, and adrenal hemorrhage.
Manifestations of Addison disease are related to
hypocortisolism and hypoaldosteronism. Symptoms include weakness, fatigability, hypoglycemia and related metabolic problems, lowered response to stressors, vitiligo, hyperpigmentation, and manifestations of hypovolemia and hyperkalemia.
Secondary hypercortisolism is characterized by low to absent what, leading to what?
ACTH levels, leading to inadequate adrenal stimulation, adrenal atrophy, and decreased corticosteroid production.
The most common cause is
withdrawal of exogenous administration of glucocorticoids. Manifestations are similar to those of Addison disease, only without hyperpigmentation.
Hyperfunction of the adrenal medulla is caused by a pheochromocytoma, which is a
catecholamine-producing tumor.
Symptoms of catecholamine excess are related to their sympathetic nervous system effects and include
hypertension, palpitations, tachycardia, glucose intolerance, excessive sweating, and constipation.