Endocrine Physiology Flashcards
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).
