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