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Flashcards in Endocrine Physiology Deck (26)
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A 41-year-old woman has hypocalcemia, hyperphosphatemia, and decreased urinary phosphate excretion. Injection of parathyroid hormone (PTH) causes an increase in urinary cyclic adenosine monophosphate (cAMP). The most likely diagnosis is

(A) primary hyperparathyroidism
(B) vitamin D intoxication
(C) vitamin D deficiency
(D) hypoparathyroidism after thyroid surgery
(E) pseudohypoparathyroidism

The answer is D [VII B 3 b].

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.


Which of the following hormones acts on its target tissues by a steroid hormone mechanism of action?

(A) Thyroid hormone
(B) Parathyroid hormone (PTH)
(C) Antidiuretic hormone (ADH) on the collecting duct
(D) β1 adrenergic agonists
(E) Glucagon

The answer is A [II E; Table 7.2].

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 (V2 receptors) is mediated by cyclic adenosine monophosphate (cAMP), although the other action of ADH (vascular smooth muscle, V1 receptors) is mediated by inositol 1,4,5-triphosphate (IP3). Parathyroid hormone (PTH), β1 agonists, and glucagon all act through cAMP mechanisms of action.


A 38-year-old man who has galactorrhea is found to have a prolactinoma. His physician treats him with bromocriptine, which eliminates the galactorrhea. The basis for the therapeutic action of bromocriptine is that it

(A) antagonizes the action of prolactin on the breast
(B) enhances the action of prolactin on the breast
(C) inhibits prolactin release from the anterior pituitary
(D) inhibits prolactin release from the hypothalamus
(E) enhances the action of dopamine on the anterior pituitary

The answer is C [III B 4 a (1), c (2)].

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.


Which of the following hormones originates in the anterior pituitary?

(A) Dopamine
(B) Growth hormone–releasing hormone (GHRH)
(C) Somatostatin
(D) Gonadotropin-releasing hormone (GnRH)
(E) Thyroid-stimulating hormone (TSH)
(F) Oxytocin
(G) Testosterone

The answer is E [III B; Table 7.1].

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.


Which of the following functions of the Sertoli cells mediates negative feedback control of follicle-stimulating hormone (FSH) secretion?

(A) Synthesis of inhibin
(B) Synthesis of testosterone
(C) Aromatization of testosterone
(D) Maintenance of the blood–testes barrier

The answer is A [IX B 2, 3].

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.


Which of the following substances is derived from proopiomelanocortin (POMC)?

(A) Adrenocorticotropic hormone (ACTH)
(B) Follicle-stimulating hormone (FSH)
(C) Melatonin
(D) Cortisol
(E) Dehydroepiandrosterone

The answer is A [III B 1, 2; Figure 7.5].

Proopiomelanocortin (POMC) is the parent molecule in the anterior pituitary for adrenocorticotropic hormone (ACTH), β-endorphin, α-lipotropin, and β-lipotropin (and in the intermediary lobe for melanocyte-stimulating hormone [MSH]). Follicle-stimulating hormone (FSH) is not a member of this “family”; rather, it is a member of the thyroid-stimulating 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.


Which of the following inhibits the secretion of growth hormone by the anterior pituitary?

(A) Sleep
(B) Stress
(C) Puberty
(D) Somatomedins
(e) Starvation
(f) Hypoglycemia

The answer is D [III B 3 a].

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).


Selective destruction of the zona glomerulosa of the adrenal cortex would produce a deficiency of which hormone?

(A) Aldosterone
(B) Androstenedione
(C) Cortisol
(D) Dehydroepiandrosterone
(E) Testosterone

The answer is A [V A 1; Figure 7.10].

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.


Which of the following explains the suppression of lactation during pregnancy?

(A) Blood prolactin levels are too low for milk production to occur
(B) Human placental lactogen levels are too low for milk production to occur
(C) The fetal adrenal gland does not produce sufficient estriol
(D) Blood levels of estrogen and progesterone are high
(E) The maternal anterior pituitary is suppressed

The answer is D [X F 5].

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.


Which step in steroid hormone biosynthesis, if inhibited, blocks the production of all androgenic compounds but does not block the production of glucocorticoids?

(A) Cholesterol → pregnenolone
(B) Progesterone → 11-deoxycorticosterone
(C) 17-Hydroxypregnenolone → dehydroepiandrosterone
(D) Testosterone → estradiol
(E) Testosterone → dihydrotestosterone

The answer is C [Figure 7.11].

The conversion of 17-hydroxypregnenolone to dehyd-roepiandrosterone (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.


A 46-year-old woman has hirsutism, hyperglycemia, obesity, muscle wasting, and increased circulating levels of adrenocorticotropic hormone (ACTH). The most likely cause of her symptoms is

(A) primary adrenocortical insufficiency (Addison disease)
(B) pheochromocytoma
(C) primary overproduction of ACTH (Cushing disease)
(D) treatment with exogenous glucocorticoids
(e) hypophysectomy

The answer is C [V A 5 b].

This woman has the classic symptoms of a primary elevation of adrenocorticotropic hormone (ACTH) (Cushing 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 disease is caused by primary adrenocortical insufficiency. Although a patient with Addison 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.


Which of the following decreases the conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol?

(A) A diet low in Ca2+
(B) Hypocalcemia
(C) Hyperparathyroidism
(D) Hypophosphatemia
(E) Chronic renal failure

The answer is E [VII C 1].

Ca2+ deficiency (low Ca2+ diet or hypocalcemia) activates 1α-hydroxylase, 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.


Increased adrenocorticotropic hormone (ACTH) secretion would be expected in patients

(A) with chronic adrenocortical insufficiency (Addison disease)
(B) with primary adrenocortical hyperplasia
(C) who are receiving glucocorticoid for immunosuppression after a renal transplant
(D) with elevated levels of angiotensin II

The answer is A [V A 2 a (3); Table 7.6; Figure 7.12].

Addison 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.


Which of the following would be expected in a patient with Graves disease?

(A) Cold sensitivity
(B) Weight gain
(C) Decreased O2 consumption
(D) Decreased cardiac output
(E) Drooping eyelids
(F) Atrophy of the thyroid gland
(G) Increased thyroid-stimulating hormone (TSH) levels
(H) Increased triiodothyronine (T3) levels

The answer is H [IV B 2; Table 7.5].

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 (T3) 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 O2 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.


Blood levels of which of the following substances is decreased in Graves disease?

(A) Triiodothyronine (T3)
(B) Thyroxine (T4)
(C) Diiodotyrosine (DIT)
(D) Thyroid-stimulating hormone (TSH)
(E) Iodide (I−)

The answer is D [IV B 2; Table 7.5].

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).


Which of the following hormones acts by an inositol 1,4,5-triphosphate (IP3)-Ca2+ mechanism of action?

(A) 1,25-Dihydroxycholecalciferol
(B) Progesterone
(C) Insulin
(D) Parathyroid hormone (PTH)
(E) Gonadotropin-releasing hormone (GnRH)

The answer is E [Table 7.2].

Gonadotropin-releasing hormone (GnRH) is a peptide hormone that acts on the cells of the anterior pituitary by an inositol 1,4,5-triphosphate (IP3)-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 cyclase–cyclic adenosine monophosphate (cAMP) mechanism.


Which step in steroid hormone biosynthesis is stimulated by adrenocorticotropic hormone (ACTH)?

(A) Cholesterol → pregnenolone
(B) Progesterone → 11-deoxycorticosterone
(C) 17-Hydroxypregnenolone → dehydroepiandrosterone
(D) Testosterone → estradiol
(E) Testosterone → dihydrotestosterone

The answer is A [V A 2 a (2)].

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 source of estrogen during the second and third trimesters of pregnancy is the

(A) corpus luteum
(B) maternal ovaries
(C) fetal ovaries
(D) placenta
(E) maternal ovaries and fetal adrenal gland
(F) maternal adrenal gland and fetal liver
(G) fetal adrenal gland, fetal liver, and placenta

The answer is G [X F 3].

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.


Which of the following causes increased aldosterone secretion?

(A) Decreased blood volume
(B) Administration of an inhibitor of angiotensin-converting enzyme (ACE)
(C) Hyperosmolarity
(D) Hypokalemia

The answer is A [V A 2 b].

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 II. Hyperosmolarity stimulates antidiuretic hormone (ADH) (not aldosterone) secretion. Hyperkalemia, not hypokalemia, directly stimulates aldosterone secretion by the adrenal cortex.


Secretion of oxytocin is increased by

(A) milk ejection
(B) dilation of the cervix
(C) increased prolactin levels
(D) increased extracellular fluid (ECF) volume
(E) increased serum osmolarity

The answer is B [III C 2].

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).


A 61-year-old woman with hyperthyroidism is treated with propylthiouracil. The drug reduces the synthesis of thyroid hormones because it inhibits oxidation of

(A) Triiodothyronine (T3)
(B) Thyroxine (T4)
(C) Diiodotyrosine (DIT)
(D) Thyroid-stimulating hormone (TSH)
(E) Iodide (I−)

The answer is E [IV A 2].

For iodide (I−) to be “organified” (incorporated into thyroid hormone), it must be oxidized to I2, which is accomplished by a peroxidase enzyme in the thyroid follicular cell membrane. Propylthiouracil inhibits peroxidase and, therefore, halts the synthesis of thyroid hormones.


A 39-year-old man with untreated diabetes mellitus type I is brought to the emergency room. An injection of insulin would be expected to cause an increase in his

(A) urine glucose concentration
(B) blood glucose concentration
(C) blood K+ concentration
(D) blood pH
(E) breathing rate

The answer is D [VI C 3; Table 7.7].

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 K+ 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.


Which of the following results from the action of parathyroid hormone (PTH) on the renal tubule?

(A) Inhibition of 1α-hydroxylase
(B) Stimulation of Ca2+ reabsorption in the distal tubule
(C) Stimulation of phosphate reabsorption in the proximal tubule
(D) Interaction with receptors on the luminal membrane of the proximal tubular cells (e) Decreased urinary excretion of cyclic adenosine monophosphate (CAMP)

The answer is B [VII B 2].

Parathyroid hormone (PTH) stimulates both renal Ca2+ reabsorption in the renal distal tubule and the 1α-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.


Which step in steroid hormone biosynthesis occurs in the accessory sex target tissues of the male and is catalyzed by 5α-reductase?

(A) Cholesterol → pregnenolone
(B) Progesterone → 11-deoxycorticosterone
(C) 17-Hydroxypregnenolone → dehydroepiandrosterone
(D) Testosterone → estradiol
(E) Testosterone → dihydrotestosterone

The answer is E [IX A].

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


Which of the following pancreatic secretions has a receptor with four subunits, two of which have tyrosine kinase activity?

(A) Insulin
(B) Glucagon
(C) Somatostatin
(D) Pancreatic lipase

The answer is A [VI C 2].

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


A 16-year-old, seemingly normal female is diagnosed with androgen insensitivity disorder. She has never had a menstrual cycle and is found to have a blind-ending vagina; no uterus, cervix, or ovaries; a 46 XY genotype; and intra-abdominal testes. Her serum testosterone is elevated. Which of the following characteristics is caused by lack of androgen receptors?

(A) 46 XY genotype
(B) Testes
(C) Elevated serum testosterone
(D) Lack of uterus and cervix
(E) Lack of menstrual cycles

The answer is C [IX C].

The elevated serum testosterone is due to lack of androgen receptors on the anterior pituitary (which normally would mediate negative feedback by testosterone). The presence of testes is due to the male genotype. The lack of uterus and cervix is due to anti-müllerian hormone (secreted by the fetal testes), which suppressed differentiation of the müllerian ducts into the internal female genital tract. The lack of menstrual cycles is due to the absence of a female reproductive tract.