BRS Endocrine Physiology Quiz: Trivia!

Proopiomelanocortin (POMC) is the parent molecule in the anterior pituitary for adrenocorticotropic hormone (ACTH), 13-endorphin, a-lipotropin, and [3-lipotropin [and in the intermediary lobe for melanocyte-stimulating hormone (MSH)]. Folliclestimulating hormone (FSH) is not a member of this "family"; rather, it is a member of the thyroidstimulating hormone (TSH) and luteinizing hormone (LH) "family." MSH, a component of POMC and ACTH, may stimulate melatonin production. Cortisol and dehydroepiandrosterone are produced by the adrenal cortex.

Aldosterone is produced in the zona glomerulosa of the adrenal cortex because that layer contains the enzyme for conversion of corticosterone to aldosterone (aldosterone synthase). Cortisol is produced in the zona fasciculata. Androstenedione and dehydroepiandrosterone are produced in the zona reticularis. Testosterone is produced in the testes, not in the adrenal cortex.

Thyroid-stimulating hormone (TSH) is secreted by the anterior pituitary. Dopamine, growth hormone releasing hormone (GHRH), somatostatin, and gonadotropin-releasing hormone (GnRH) all are secreted by the hypothalamus. Oxytocin is secreted by the posterior pituitary. Testosterone is secreted by the testes.

Parathyroid hormone (PTH) stimulates both renal Ca 2+ reabsorption in the renal distal tubule and the la-hydroxylase enzyme. PTH inhibits (not stimulates) phosphate reabsorption in the proximal tubule, which is associated with an increase in urinary cyclic adenosine monophosphate (cAMP). The receptors for PTH are located on the basolateral membranes, not the luminal membranes.

Although the high circulating levels of estrogen stimulate prolactin secretion during pregnancy, the action of prolactin on the breast is inhibited by progesterone and estrogen. After parturition, progesterone and estrogen levels decrease dramatically. Prolactin can then interact with its receptors in the breast, and lactation proceeds if initiated by suckling.

The conversion of 17-hydroxypregnenolone to dehydroepiandrosterone (as well as the conversion of 17-hydroxyprogesterone to androstenedione) is catalyzed by 17,20-lyase. If this process is inhibited, synthesis of androgens is stopped

This woman has the classic symptoms of a primary elevation of adrenocorticotropic hormone (ACTH) [Cushing's disease]. Elevation of ACTH stimulates overproduction of glucocorticoids and androgens. Treatment with pharmacologic doses of glucocorticoids would produce similar symptoms, except that circulating levels of ACTH would be low because of negative feedback suppression at both the hypothalamic [corticotropin-releasing hormone (CRH)] and anterior pituitary (ACTH) levels. Addison's disease is caused by primary adrenocortical insufficiency. Although a patient with Addison's disease would have increased levels of ACTH (because of the loss of negative feedback inhibition), the symptoms would be of glucocorticoid deficit, not excess. Hypophysectomy would remove the source of ACTH. A pheochromocytoma is a tumor of the adrenal medulla that secretes catecholamines.

The insulin receptor in target tissues is a tetramer. The two 13 subunits have tyrosine kinase activity and autophosphorylate the receptor when stimulated by insulin.

Thyroid hormone, an amine, acts on its target tissues by a steroid hormone mechanism, inducing the synthesis of new proteins. The action of antidiuretic hormone (ADH) on the collecting duct (V 2 receptors) is mediated by cyclic adenosine monophosphate (cAMP), although the other action of ADH (vascular smooth muscle, V 1 receptors) is mediated by inositol 1,4,5-triphosphate (IP 3). Parathyroid hormone (PTH), 13 1 agonists, and glucagon all act through cAMP mechanisms of action.

Curve A shows basal body temperature. The increase in temperature occurs as a result of elevated progesterone levels during the luteal (secretory) phase of the menstrual cycle. Progesterone increases the set-point temperature in the hypothalamic thermoregulatory center.

The curve shows blood levels of estradiol. During the luteal phase of the cycle, the source of the estradiol is the corpus luteum. The corpus luteum prepares the uterus to receive a fertilized egg.

In Graves' disease (hyperthyroidism), the thyroid is stimulated to produce and secrete vast quantities of thyroid hormones as a result of stimulation by thyroid-stimulating immunoglobulins [antibodies to the thyroid-stimulating hormone (TSH) receptors on the thyroid gland]. Because of the high circulating levels of thyroid hormones, anterior pituitary secretion of TSH will be turned off (negative feedback).

Some target tissues for androgens contain 5a-reductase, which converts testosterone to dihydrotestosterone, the active form in those tissues.

Progesterone is secreted during the luteal phase of the menstrual cycle.

Low blood [Ca2+] and high blood [phosphate] are consistent with hypoparathyroidism. Lack of parathyroid hormone (PTH) decreases bone resorption, decreases renal reabsorption of Ca2+ , and increases renal reabsorption of phosphate (causing low urinary phosphate). Because the patient responded to exogenous PTH with an increase in urinary cyclic adenosine monophosphate (cAMP), the G protein coupling the PTH receptor to adenylate cyclase is apparently normal. Consequently, pseudohypoparathyroidism is excluded. Vitamin D intoxication would cause hypercalcemia, not hypocalcemia. Vitamin D deficiency would cause hypocalcemia and hypophosphatemia.

Suckling and dilation of the cervix are the physiologic stimuli for oxytocin secretion. Milk ejection is the result of oxytocin action, not the cause of its secretion. Prolactin secretion is also stimulated by suckling, but prolactin does not directly cause oxytocin secretion. Increased extracellular fluid (ECF) volume and hyperosmolarity are the stimuli for the secretion of the other posterior pituitary hormone, antidiuretic hormone (ADH).

Graves' disease (hyperthyroidism) is caused by overstimulation of the thyroid gland by circulating antibodies to the thyroid-stimulating hormone (TSH) receptor [which then increases the production and secretion of triiodothyronine (T 3) and thyroxine (T4), just as TSH would]. Therefore, the signs and symptoms of Graves' disease are the same as those of hyperthyroidism, reflecting the actions of increased circulating levels of thyroid hormones: increased heat production, weight loss, increased 02 consumption and cardiac output,
exophthalmos (bulging eyes, not drooping eyelids), and hypertrophy of the thyroid gland (goiter). TSH levels will be decreased (not increased) as a result of the negative feedback effect of increased T3 levels on the anterior pituitary.

Inhibin is produced by the Sertoli cells of the testes when they are stimulated by follicle-stimulating hormone (FSH). Inhibin then inhibits further secretion of FSH by negative feedback on the anterior pituitary. The Leydig cells synthesize testosterone. Testosterone is aromatized in the ovaries.

Growth hormone is secreted in pulsatile fashion, with a large burst occurring during deep sleep (sleep stage 3 or 4). Growth hormone secretion is increased by sleep, stress, puberty, starvation, and hypoglycemia. Somatomedins are generated when growth hormone acts on its target tissues; they inhibit growth hormone secretion by the anterior pituitary, both directly and indirectly (by stimulating somatostatin release).

For iodide (I-) to be "organified" (incorporated into thyroid hormone), it must be oxidized to 1 2, which is accomplished by a peroxidase enzyme in the thyroid follicular cell membrane. Propylthiouracil inhibits peroxidase and, therefore, halts the synthesis of thyroid hormones.

Decreased blood volume stimulates the secretion of renin (because of decreased renal perfusion pressure) and initiates the renin-angiotensin-aldosterone cascade. Angiotensin-converting enzyme (ACE) inhibitors block the cascade by decreasing the production of angiotensin Hyperosmolarity stimulates antidiuretic hormone (ADH) [not aldosterone] secretion. Hyperkalemia, not hypokalemia, directly stimulates aldosterone secretion by the adrenal cortex.

Before the injection of insulin, the woman would have had hyperglycemia, glycosuria, hyperkalemia, and metabolic acidosis with compensatory hyperventilation. The injection of insulin would be expected to decrease her blood glucose (by increasing the uptake of glucose into the cells), decrease her urinary glucose (secondary to decreasing her blood glucose), decrease her blood K+ (by shifting 1C+ into the cells), and correct her metabolic acidosis (by decreasing the production of ketoacids). The correction of the metabolic acidosis will lead to an increase in her blood pH and will reduce her compensatory hyperventilation.

The conversion of cholesterol to pregnenolone is catalyzed by cholesterol desmolase. This step in the biosynthetic pathway for steroid hormones is stimulated by adrenocorticotropic hormone (ACTH).

The curve shows blood levels of estradiol. The source of the increase in estradiol concentration shown at point C is the ovarian granulosa cells, which contain high concentrations of aromatase and convert testosterone to estradiol.

Addison's disease is caused by primary adrenocortical insufficiency. The resulting decrease in cortisol production causes a decrease in negative feedback inhibition on the hypothalamus and the anterior pituitary. Both of these conditions will result in increased adrenocorticotropic hormone (ACTH) secretion. Patients who have adrenocortical hyperplasia or who are receiving exogenous glucocorticoid will have an increase in the negative feedback inhibition of ACTH secretion.

Bromocriptine is a dopamine agonist. The secretion of prolactin by the anterior pituitary is tonically inhibited by the secretion of dopamine from the hypothalamus. Thus, a dopamine agonist acts just like dopamine—it inhibits prolactin secretion from the anterior pituitary

Ca2÷ deficiency (low Ca 2+ diet or hypocalcemia) activates lahydroxylase,
which catalyzes the conversion of vitamin D to its active form, 1,25-dihydroxycholecalciferol. Increased parathyroid hormone (PTH) and hypophosphatemia also stimulate the enzyme. Chronic renal failure is associated with a constellation of bone diseases, including osteomalacia caused by failure of the diseased renal tissue to produce the active form of vitamin D.

Point E shows the luteinizing hormone (LH) surge that initiates ovulation at mid-cycle. The LH surge is caused by increasing estrogen levels from the developing ovarian follicle. Increased estrogen, by positive feedback, stimulates the anterior pituitary to secrete LH and follicle-stimulating hormone (FSH).

During the second and third trimesters of pregnancy, the fetal adrenal gland synthesizes dehydroepiandrosterone-sulfate (DHEA-S), which is hydroxylated in the fetal liver and then transferred to the placenta, where it is aromatized to estrogen. In the first trimester, the corpus luteum is the source of both estrogen and progesterone.

Gonadotropin-releasing hormone (GnRH) is a peptide hormone that acts on the cells of the anterior pituitary by an inositol 1,4,5-triphosphate (IP 3)-Ca2+ mechanism to cause the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). 1,25-Dihydroxycholecalciferol and progesterone are steroid hormone derivatives of cholesterol that act by inducing the synthesis of new proteins. Insulin acts on its target cells by a tyrosine kinase mechanism. Parathyroid hormone (PTH) acts on its target cells by an adenylate cyclasecyclic adenosine monophosphate (cAMP) mechanism.