Review Questions
1. The major mechanism for endocrine homeostasis is
A. neurotransmitters blocking hormone receptors.
B. one hormone antagonizing the action of another hormone.
C. positive feedback to accelerate a response.
D. negative feedback of output onto input.
E. by release of hypothalamic hormones.
2. Growth hormone (GH)
A. decreases amino acid transport into cells.
B. increases free fatty acids in plasma.
C. release is decreased by glucagon.
D. release is decreased by exercise.
E. directly stimulates bone growth.
3. Prolactin secretion
A. comes from the posterior pituitary.
B. suppresses gonadotropin-releasing hormone (GnRH).
C. stimulates glycogenolysis.
D. stimulates gluconeogenesis.
E. peaks early in pregnancy.
4. Oxytocin
A. stimulates mammary myoepithelial contraction.
B. stimulates myometrial contraction when plasma progesterone levels are high.
C. stimulates the production of neurophysin by the liver.
D. is a prolactin release–inhibiting factor.
E. initiates labor.
5. Which is the most important factor in controlling vasopressin (antidiuretic hormone, ADH) secretion?
A. Blood pressure
B. Plasma osmolality
C. Blood volume
D. Angiotensin II
E. Stress
6. One-half hour after the cessation of a release episode producing normal plasma levels of the following hormones, which one will have the highest level?
A. Cortisol
B. Adrenocorticotropin hormone (ACTH)
C. Epinephrine
D. Thyroxine (T4)
E. Aldosterone
7. An inhibitor of thyroid peroxidase may
A. inhibit intracellular binding of triiodothyronine (T3).
B. inhibit intracellular binding of T4.
C. result in hypothyroidism.
D. increase iodide uptake into the thyroid gland.
E. diminish the sensitivity of pituitary cells to thyrotropin-releasing hormone.
8. Which of the following are characteristic of thyroxine (T4)?
A. Less than 50% of the hormone in circulation is bound to plasma protein.
B. Its half-life in blood is < 1 hour.
C. Large amounts are stored intracellularly.
D. Conversion to triiodothyronine (T3) takes place within target tissue cells.
E. Its release is directly controlled by thyrotropin-releasing hormone (TRH).
Questions 9 to 11 refer to the clinical scenario that follows. A 43-year-old man presents with lethargy and sleepiness; dry, scaly skin; sparse, dry hair; dull expression with droopy eyelids; bradycardia (60 beats/min); blood pressure of 90/70; hematocrit of 27; enlarged heart; constipation; and hypothermia. Plasma concentrations of thyroxine (T4) and triiodothyronine (T3) reveal a total T4 of 2.5 μg/dL, whereas normal is 5 to 14 μg/dL. Peripheral blood has elevated levels of thyroid-stimulating hormone (TSH) levels.
9. This patient has which of the following?
A. Addison disease
B. Cushing disease
C. Hyperthyroidism
D. Hypothyroidism
E. Type II diabetes
10. What defect might be responsible for these symptoms?
A. Reduced synthesis of TSH
B. Reduced synthesis of TRH
C. Reduced synthesis of thyroid hormone
D. Increased release of thyroid hormone
E. Lack of nuclear thyroid hormone receptors
11. What is the best treatment for this patient?
A. Iodinated salt
B. Thyroid hormone (T4)
C. Surgery to remove a thyroid tumor, a common cause of hyperthyroidism, or drug treatment to suppress excess production of T4
D. Cortisol
E. Insulin
12. Hyperparathyroidism is characterized by
A. Ca2+ kidney stones and gallstones.
B. convulsions.
C. parethesias.
D. numbness.
E. tetany.
13. Calcitonin
A. secretion is stimulated by low plasma [Ca2+].
B. promotes bone formation.
C. has membrane receptors in the intestine.
D. decreases urinary excretion of Ca2+ and phosphate.
E. is an effective treatment for osteoporosis in postmenopausal women.
For Questions 14–16
A 55-year-old woman had a total thyroidectomy followed by thyroid hormone replacement. Forty-eight hours later, she developed laryngea l spasms, tetany, and cramps in her hands. Laboratory tests showed reduced plasma Ca2+and elevated plasma PO43−.
Daily oral calcium gluconate and vitamin D were given to alleviate her symptoms.
14. What is the patient’s endocrinopathy?
A. Increased renal clearance of Ca2+
B. Excess cortisol
C. Decreased stimulation of the anterior pituitary
D. Lack of adequate thyroid hormone
E. Lack of parathyroid hormone
15. Vitamin D is given with the calcium (Ca2+) gluconate because vitamin D
A. increases absorption of Ca2+ by the gut.
B. binds to the Ca2+ in the gut.
C. prevents destruction of Ca2+ in the stomach.
D. makes the Ca2+ gluconate more stable in solution.
E. decreases intestinal absorption of PO43−.
16. What caused the tetany and muscle spasms?
A. Hypercalcemia
B. Hypocalcemia
C. Hypophosphatemia
D. Hyperphosphatemia
E. Lack of vitamin D
17. In humans, total adrenalectomy is fatal without replacement therapy. Hypophysectomy (surgical removal of the pituitary gland) is not fatal, because in hypophysectomy
A. the adrenal cortex undergoes compensatory hypertrophy.
B. the secretion of aldosterone is normal.
C. adrenal catecholamines compensate for the metabolic actions of cortisol.
D. tissue requirements for corticosteroids fall to low levels.
E. plasma concentration of angiotensin II increases.
18. Giving a patient a drug that inhibits angiotensin-converting enzyme (ACE) will increase which of the following?
A. Plasma concentration of angiotensin II
B. Na+ clearance
C. K+ clearance
D. Peripheral resistance
E. Secretion of renin
19. A drug that prevents the binding of dexamethasone to glucocorticoid receptors would cause which outcome?
A. A negative nitrogen balance
B. Decreased concentration of adrenocorticotropic hormone (ACTH) in the blood
C. Decreased concentration of cortisol in the blood
D. Increased concentration of insulin in the blood
E. Decreased concentration of cortisol in cell nuclei
20. Treatment of a normal person with large amounts of cortisol causes
A. decreased hepatic glycogen content.
B. skeletal muscle anabolism.
C. increased adrenal size.
D. central deposition of fat.
E. resistance to peptic ulcers.
21. The synthesis of epinephrine depends on
A. angiotensin II secretion.
B. local cortisol concentration.
C. dehydroepiandrosterone (DHEA).
D. an intact zona glomerulosa.
E. 11β–hydroxylase.
22. Secretion of catecholamines by cells of the adrenal medulla depends on
A. the increased concentration of Ca2+ in the cytoplasm.
B. exocytosis of calmodulin.
C. inactivation of the release of somatostatin.
D. hyperpolarization of the cell membrane.
E. the release of norepinephrine from preganglionic sympathetic neurons.
23. Stimulation of cyclic adenosine monophosphate (cAMP) by epinephrine in target cells
A. requires translocation of epinephrine into the nucleus.
B. is mediated by a protein that binds guanosine triphosphate (GTP).
C. is amplified by prior long-term exposure of cells to norepinephrine.
D. is inversely related to the number of adrenergic receptors present on the cell.
E. depends on the internalization of epinephrine-receptor complexes.
24. Ca2+ influx into pancreatic β cells
A. is the result of stopping the Na+−K+ ATPase pump.
B. causes glucose to enter the cells.
C. stimulates release of glucagon.
D. activates calmodulin.
E. slows insulin synthesis.
25. Glucagon
A. increases insulin secretion.
B. operates through G proteins to increase cAMP.
C. decreases gluconeogenesis.
D. decreases lipolysis.
E. decreases glycogenolysis.
26. If somatostatin were given with a β-blocker, what would you expect the plasma glucose response to be over the next 2 hours?
A. Plasma glucose concentration would decrease.
B. Plasma glucose concentration would increase.
C. Plasma glucose concentration would decrease, then increase.
D. Plasma glucose concentration would increase, then decrease.
E. Plasma glucose concentration would not change.
For Questions 27−30
A patient with type I diabetes is found in a coma. Blood glucose, urine glucose, blood ketones, and urine ketones are all elevated; serum HCO3− is < 12 mEq/L. Respirations are quick and deep with acetone breath. Blood pressure is 95/61 mm Hg, and the pulse is weak and rapid (119 beats/min).
27. What is the condition of this person?
A. Ketoacidosis
B. Insulin shock
C. Heat stroke
D. Heat exhaustion
E. Adrenocortical insufficiency
28. What factor in this patient’s condition is the major cause of their low serum HCO3−?
A. The patient has been hyperventilating.
B. The patient has been excreting acidic urine.
C. It has been depleted to buffer ketoacids.
D. The patient has compensated for the low CO2.
E. The patient tries to achieve a normal [HCO3−]/Pco2 ratio.
29. What is the cause of the patient’s dyspnea, tachycardia, and hypotension?
A. Plasma hyperglycemia
B. High urine glucose
C. Blood ketosis
D. Urine ketosis
E. Blood acidosis
30. What would you expect the plasma glucose response to be over the next 2 hours after giving insulin?
A. Plasma glucose concentration would decrease.
B. Plasma glucose concentration would increase.
C. Plasma glucose concentration would decrease, then increase.
D. Plasma glucose concentration would increase, then decrease.
E. Plasma glucose would remain high.
31. What is the major energy source for the body after 48 hours of fasting?
A. Muscle protein
B. Liver glycogen
C. Muscle glycogen
D. Triglycerides
E. Glucose
Answers and Explanations
1. D. Negative feedback control produces a relatively stable level of hormone in the bloodstream (p. 243).
A Neurotransmitters rarely block hormone receptors.
B Hormones do antagonize one another and minimize actions, but this does not produce stability.
C Positive feedback produces explosive responses, not stability.
E Most hypothalamic hormones cause release of other hormones, but their control depends on negative feedback.
2. B. Growth hormone (GH) increases lipolysis in the presence of cortisol (p. 248). This increases free fatty acids in plasma.
A GH increases amino acid transport into cells.
C,D GH release is stimulated by both glucagon and exercise.
E Bone growth is stimulated indirectly by insulinlike growth factor (IGF).
3. B. Prolactin secretion suppresses GnRH. This causes lactation amenorrhea, so nursing mothers are unlikely to become pregnant (p. 249).
A Prolactin is secreted from the anterior pituitary.
C,D Prolactin secretion stimulates galactopoiesis (the secretion and continued production of milk by the mammary glands) rather than production of glucose or breakdown of glycogen in the liver.
E Prolactin levels peak 2 weeks before term and then decrease, but they are increased by each session of suckling.
4. A. Oxytocin stimulates the contraction of the myoepithelial cells of the mammary glands (p. 250).
B Oxytocin stimulates the contraction of an “estrogenized,” not “progesteronized,” uterus.
C Neurophysin is produced in hypothalamic nuclei, not in the liver.
D Oxytocin is a prolactin-releasing factor.
E Oxytocin participates in but does not initiate labor.
5. B. Plasma osmolality is the most potent factor in controlling vasopressin secretion (p. 250).
A,C Decrease of blood pressure or blood volume will also cause the release of greater qualities of ADH.
D,E Angiotensin II and stress will also affect ADH release indirectly.
6. D. Thyroxine has the longest half-life (5−7 days) and will therefore have the highest level (p. 243).
A,E Steroid hormones (e.g., ACTH and aldosterone) are largely
bound to plasma proteins, so they have a half-life of 1 or 2 hours.
B Protein hormones have a half-life of several minutes.
C Catecholamines have a half-life < 1 minute.
7. C. Inhibition of thyroid peroxidase depresses thyroxine synthesis, producing hypothyroidism (p. 252).
A, B Inhibition of thyroid peroxidase does not inhibit intracellular binding of T3 or T4.
D,E Inhibition of thyroid peroxidase does not affect iodide uptake or sensitivity of pituitary cells.
8. D. Thyroxine (T4) is converted to triiodothyronine (T3) within target tissue cells. T3 is the more active form of thyroid hormone (p. 254).
A,B T4 is > 99% bound to transport proteins in plasma and has a half-life of 7 days.
C T4 is stored as thyroglobulin extracellularly in the lumen of the follicle.
E TRH acts in the anterior pituitary to control release of thyroidstimulating hormone, which then acts on the thyroid gland to release T3and T4.
9. D. He has the symptoms of hypothyroidism (myxedema).
A Addison disease has a few of the same symptoms. It is caused by a lack of cortisol.
B Cushing disease has different symptoms. It is caused by excess cortisol.
C In hyperthyroidism, metabolism and heat production are raised.
E Diabetic patients show drowsiness but none of the other symptoms.
10. C. Low levels of T4 suggest impaired synthesis (p. 255).
A TSH production is elevated due to disinhibition.
B TRH release must be normal and above normal to elevate levels of TSH.
D TRH release is a consequence of low T4, not the primary pathology.
E The low levels of T4 are sufficient to explain the symptoms without a lack of nuclear thyroid hormone receptors.
11. B. Replacement with thyroxine (T4) will treat the patient’s symptoms (p. 255).
A Thyroxine synthesis is operating, so it is unlikely that iodine is limiting.
C A hypothalamic or pituitary tumor may be the primary cause, but it is not the only cause of reduced TSH.
D Cortisol is required for treatment of Addison disease, not secondary hypothyroidism.
E Insulin is the treatment for diabetes.
12. A. Hyperparathyroidism causes high plasma [Ca2+], which leads to kidney stones and gallstones (p. 263).
B–E All the other choices occur with hypoparathyroidism and low plasma [Ca2+], which destabilizes membranes of nerve and muscle cells.
13. E. Calcitonin inhibits bone reabsorption and is thus an effective treatment for osteoporosis in postmenopausal women (p. 266).
A Calcitonin secretion is stimulated by high plasma Ca2+.
B Calcitonin has no effect on bone formation.
C Calcitonin has membrane receptors on osteoclasts and renal tubule cells.
D Calcitonin increases urinary excretion of Ca2+ and phosphate.
14. E. Lack of parathyroid hormone causes reduced plasma Ca2+ and elevated plasma PO43−(p. 262).
A Increased renal clearance of Ca2+ cannot reduce plasma Ca2+ enough to produce these symptoms.
B Excess cortisol (Cushing disease) produces obesity and muscle wasting.
C Parathyroid hormone is not regulated by the pituitary.
D There are no symptoms of a lack of thyroid hormone with its replacement.
15. A. Calcitriol (vitamin D) increases the active transporters of Ca2+ and increases Ca2+ permeability of the small intestine (p. 265).
B Calcitriol does not bind to Ca2+ in the gut.
C Ca2+ is not destroyed in the stomach.
D Calcitriol does not make Ca2+ gluconate more stable; Ca2+ is more easily absorbed from the gluconate salt than from Ca2+ carbonate.
E Calcitriol increases absorption of PO43−.
16. B. Hypocalcemia (low plasma Ca2+) reduces the stability of skeletal muscle membranes, so they fire repetitive action potentials spontaneously (p. 260).
A Hypercalcemia (high plasma Ca2+) makes excitable membranes more stable.
C–E Hypophosphatemia (low plasma PO43−), hyperphosphatemia (high plasma PO43−), and vitamin D have little effect on excitable membranes.
17. B. Aldosterone secretion is normal because it is regulated by plasm a [K+] and angiotensin, not the hypothalamus–pituitary−adrenal axis (pp. 270, 271).
A The adrenal cortex atrophies after hypophysectomy.
C Catecholamines and cortisol have different spectra of actions.
D Requirement for corticosteroids rises when their release is suppressed.
E Angiotensin II levels are unchanged.
18. B. ACE inhibitors slow formation of angiotensin II (A) and reduce aldosterone secretion. Less aldosterone produces less Na+ reabsorption, so Na+ clearance increases (pp. 270, 271).
C K+ secretion is also reduced, so K+ clearance decreases.
D Less vasoconstrictor action of angiotensin II produces decreased peripheral resistance.
E Secretion of renin is unchanged.
19. E. Steroids act upon target cells by binding to a cytoplasmic receptor, which is transported into the nucleus, where it induces or represses gene transcription. A glucocorticoid receptor blocker prevents cortisol from having its normal mechanism of action.
A Decreased cortisol activity produces a positive nitrogen balance as tissue is metabolized.
B,C Symptoms of decreased ACTH or cortisol (Addison disease) are similar to those with blocked receptors, but they are not caused by receptor block.
D. Insulin secretion is not increased by cortisol activity.
20. D. Large amounts of cortisol causes central deposits of fat. This leads to truncal obesity, a hallmark of Cushing syndrome (p. 276).
A, B Cortisol promotes liver glycogen deposition and muscle proteolysis.
C Cortisol causes inhibition of ACTH secretion and thus decreased adrenal size.
E Cortisol promotes peptic ulcers.
21. B. Epinephrine is formed from norepinephrine by the action of the enzyme phenylethanolamine N-methyltransferase (PNMT), which is induced by cortisol (p. 276).
A Angiotensin II facilitates synthesis of aldosterone from corticosteron E.
C DHEA is a precursor for androgens.
D Epinephrine is synthesized in the adrenal medulla, not in the zona glomerulosa of the adrenal cortex.
E 11β–hydroxylase is the final enzyme in the synthesis of cortisol.
22. A. Stimulus-secretion coupling involves depolarization of the membrane (D), followed by elevated cytoplasmic Ca2+, which initiates the secretory process (p. 277).
B Calmodulin is located in muscle cells, not the adrenal medulla.
C Somatostatin has no role in secretion.
E Acetylcholine is released from preganglionic sympathetic neurons.
23. B. The binding of epinephrine to the β-adrenergic receptors results in the activation of Gs proteins, which bind GTP and subsequently activate the conversion of adenosine triphosphate (ATP) to cAMP via adenylate cyclase (p. 244).
A,C It does not require translocation of epinephrine or long-term exposure to norepinephrine.
D Stimulation is directly related to the number of adrenergic receptors.
E The Epinephrine-receptor complex remains on the cell membrane. The activated G proteins act within the cell.
24. D. Ca2+ influx into pancreatic β cells activates calmodulin and Ca2+/calmodulin-dependent protein kinase (p. 279).
A Stopping the Na+–K+ ATPase pump (due to low ATP levels for example), causes Ca2+ influx to decrease. A rise of ATP levels causes K+ channels to close, resulting in depolarization that opens voltage-gated Ca2+ channels.
B Glucose binds to a GLUT-2 transporter and enters β cells before Ca2+ does.
C,E The Ca2+ influx releases insulin (not glucagon) and increases insulin synthesis.
25. B. Glucagon activates G proteins, which stimulate an adenylate cyclase pathway to increase cAMP (pp. 283, 284).
A Glucagon decreases insulin secretion, as insulin antagonizes most of glucagon’s actions.
C–E Glucagon promotes utilization of energy stores, so it increases gluconeogenesis, lipolysis, and glycogenolysis.
26. A. Plasma glucose levels would decline due to insulin action but not return to normal due to the inhibition of glucagon secretion by somatostatin and the blockade of epinephrine action by the β-blocker.
27. A. The acetone breath is typical of ketoacidosis (p. 282).
B Insulin shock results from hypoglycemia due to excessive insulin.
C,D Heat stroke or heat exhaustion are associated with normal glucose and no elevated ketones.
E Hypoglycemia is typical of adrenocortical insufficiency (lack of cortisol).
28. C. Some of the HCO3− release buffers the ketoacids (p. 282).
A The patient’s hyperventilation slightly compensates for the acidosis and slightly reduces HCO3−.
B The patient will excrete an alkali urine.
D CO2 remains low.
E The patient’s compensation for the acidosis does not improve the [HCO3]/Pco2 ratio by reducing CO2, but that also reduces HCO3− slightly.
29. E. The acidotic state causes hyperventilation, hypotension, and tachycardia (p. 282).
A–D Ketones and glucose do not cause these symptoms.
30. C. Plasma glucose levels would decline due to insulin action, then increase (and return to normal), due to glucagon action.
31. D. Triglycerides are a potent energy source after glucose is depleted.
A Muscle protein allows amino acids to be “burned” after only 1 day, but they are less important than the breakdown of fats.
B,C Glycogen provides glucose for only 24 hours.
E Glucose in the blood is used in a few hours, although glycogenolysis keeps glucose available for almost 1 day.