Suggested reading: Chapter 77
Zona glomerulosa: Outer most layer of adrenal cortex. Very thin layer of cells on surface. Exclusive site of enzyme aldosterone synthase, major secretion is aldosterone. Lacks 17a -hydroxylase activity so it cannot synthesize cortisol and the adrenal androgens. Functions differently than the inner 2 zones (regulated by renin-angiotensin system).
Zona fasciculata: Middle layer of adrenal cortex – widest. Major secretion is cortisol (principal glucocorticoid), though does produce androgens and corticosterone in small amounts. Regulated by ACTH (excess or deficiency in this hormone alter its structure and function).
Zona reticularis: Inner zone of adrenal cortex. Secretes sex hormones and some glucocorticoids. It is stimulated by ACTH (excess or deficiency in this hormone alter its structure and function). Most prevalent adrenal androgens are dehydroepiandrosterone (DHEA) and androstenedione.
Catecholamines: Amine compound derived from catechol, such as epinephrine and norepinephrine which have sympathomimetic activity and are concerned with nervous transmission, vascular tone, and many metabolic activities. (Melloni’s Illustrated Medical Dictionary – 1993 – 3rd Edition. The Partheron Publishing Group Inc.; pg.86.)
Corticosteroids: Hormones of the adrenal cortex that are synthesized from the steroid cholesterol, they all have similar chemical formulas. Include – mineralocorticoids, glucocorticoids, androgens.
Glucocorticoids: Steroid hormone of adrenal cortex (or synthetic steroid) concerned with gluconeogenesis from amino acids and catabolism of protein. Cortisol, accounts for 95% of all glucocorticoid activity – very potent and natural occuring. Corticosterone, is 4% of total glucocorticoid activity – much less potent than cortisol. This class of compounds has other activities including anti-inflammatory activity and ability to suppress the synthesis of ACTH and MSH. Synthetic compounds include: cortisone, prednisone, methylprednisone, and dexamethasone.
Mineralocorticoids: Steroid hormones in adrenal cortex that controls salt metabolism. Includes aldosterone (very potent) which accounts for about 90% of all mineralocorticoid activity. Others include desoxycorticosterone corticosterone, 9-a Fluorocortisal (synthetic), and slight amounts of cortisol and cortisone (synthetic).
Steroidogenesis: natural production of steroids (Melloni’s Illustrated Medical Dictionary – p. 450).
CRH (corticotropin releasing hormone): Causes release of adrenocorticotropin hypothalmic releasing hormone.
ACTH (Adrenocorticotropin): Hormone from anterior pituitary that stimulates adrenal cortex to secrete adrenocortical hormones. Controls almost entire secretion of cortisol from anterior pituitary and enhances production of adrenal androgens. It is a large polypeptide, chain length of 39 amino acids. Principal effect is to activate adenyl cyclase in cell membrane. It is necessary for any adrenocortical hormone to be formed.
Cortisol (hydrocortisone): 17-hydroxycorticosterone; steroid hormone isolated from the adrenal cortex. Of natural occuring adrenal cortical hormones, it is most capable of correcting by itself the effects of adrenalectomy; provides resistance to stresses and maintains a number of enzyme systems (Melloni’s-p.112).
Corticosteroid-binding globulin (CBG, transcortin): Combines with cortisol in blood. Transported in the bound form (94%) and 6% is free. Changes in CBG’s concentration can influence measurement of total cortisol.
Permissive effect: In stressful situations glucocorticoids cause raid mobilization of amino acids and fats from cellular stores to make available for energy and synthesis of other compounds. Cortisol usually does not mobilize the basic functional proteins of cells (muscle contractile proteins and proteins of neurons) until almost all other proteins have been released. Preferential effect of cortisol could make amino acids available to needy cells to synthesize substances essential to life. (Guyton, p. 964).Does this sound right?
Cushing’s Syndrome: Clinical condition caused by hypersecretion of the glucocorticoid, cortisol.
This is either from a cortisol secreting tumor of one adrenal cortex or general hyperplasia of both adrenal cortices. Hyperplasia is usually caused by increased secretion of ACTH by the anterior pituitary or by "ectopic secretion" of ACTH by a tumor elsewhere in the body. Most abnormalities of Cushing’s Syndrome are ascribable to abnormal amounts of cortisol. Secretion of androgens is also of significance. Special characteristics include mobilization of fat from lower part of body, with concomitant extra disposition of fat in the thoracic and upper abdominal regions – "buffalo torso", edematous appearance of the face –"moon face". Androgenic potency sometimes causes acne and hirsutism (excess growth of facial hair). Eighty percent of patient’s have hypertension-presumably because of slight mineralocorticoid effects of cortisol. Enhanced gluconeogenesis (blood glucose levels increase to as high as 200mg/dl after meals) is present; and also tissue proteins are greatly decreased due to lack of protein synthesis with exception of liver and plasma proteins (ie: severe weakness-muscle; suppressed immune system –lymphoid tissue; tearing of subcutaneous tissues-diminished protein collagen fibers; osteoporosis –diminished protein deposition in bones).
Cushing’s Disease: Category of Cushing’s Syndrome that is secondary to ACTH-producing pituitary microadenomas or hypothalmic lesions. (Principles and Practice of Adult Health Nursing – Beare PG, Myers JL, The CV Mosby Co. 1990, p.1439.)
Addison’s Disease: Insufficiency of the adrenal cortex to produce adrenocortical hormones. Maybe a primary disease of the adrenal cortex or adrenocortical failure caused by a deficiency of ACTH. Frequently caused by primary atrophy of the adrenal cortices – 80% (primary atrophy) caused by autoimmunity against the cortices. Mineralocorticoid deficiency is present - lack of aldosterone secretion. Extracellular fluid volume is decreased (because of decreased renal tubular sodium reabsorption - increase sodium, chloride and water loss to urine). Develop hyponatremia, hyperkalemia, and mild acidosis. Plasma volume is decreased, RBC concentration is increased, cardiac output decreases. Patient can die off shock if untreated in 4 days to 2 weeks after cessation of mineralocorticoid secetion. Glucocorticoid deficiency is present - loss of cortisol secretion which makes it impossible to maintain normal blood glucose concentration between meals. Can’t synthesize significant quantities of glucose by gluconeogenesis. Reduces also the mobilization of proteins and fats from tissues causing depression of other metabolic functions. There is sluggishness of energy mobilization and the person is highly susceptible to deteriorating effects of stress. Melanin pigmentation is not deposited evenly but in blotches – especially in thin skin areas. This due to cortisol depression (normal negative feedback to hypothalmus and anterior pituitary also depressed). There is increased rate of ACTH secretion as well as increased amounts of MSH (increase of ACTH stimulates formation of melanin in same way as MSH). Addisonian Crisis can occur during periods of stress (trauma, disease, and surgery) due to lack of critical need of increase of glucocorticoids. Likely need excessive amounts of glucocorticoids of ten times normal quantitiy.
Dexamethasone Supression Test: Procedure for screening cortisol excess. This can be a single-dose dexamethsone suppression test (ACTH suppression test) failure to suppress cortisol production is suggestive of Cushing’s syndrome; or Standard dexamethasone suppresion test (low- dose and high-dose tests). Patient’s with Cushing’s Syndrome fail to show suppression with low doses of dexamethosone but will show suppression with high doses. Patient with adrenal carcinoma will not show suppression in either case. (Principles and Practice of Adult Health Nursing).
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