Medical Physiology

728 APPENDICES sympathetic nervous system, although they release remove 2,425 J of heat, he must secrete and evaporate acetylcholine. Sympathectomy abolishes sweating, 7 g of sweat per min. vasoconstriction, and active vasodilation. 3. The answer is C. The core temperature of a resting per- Chapter 30 son shows a circadian rhythm and is higher at 4:00 PM than at 4:00 AM. This rhythm in core temperature is the 1. The answer is C. A maximal voluntary contraction in- result of an underlying circadian rhythm in the ther- volving the identical muscles in an identical form of moregulatory set point. Because a change in the ther- contraction provides the most readily quantified and moregulatory set point affects core temperature at rest accurate basis for normalization of isometric exercise and the thresholds for sweating and vasodilation all in intensity. Choice A is incorrect because the basis for the same way, these thresholds are also higher at 4:00 comparison involves rhythmic, dynamic exercise. The PM. other choices also contradict the principle that exer- 4. The answer is E. Acclimatization to cold produces sev- cise can only be compared with other exercise involv- eral different (and contrasting) sets of changes, de- ing the same muscles and the same types of muscle pending on the acclimatizing environment (and, per- contraction. haps, on characteristics of the population being 2. The answer is A. The physiological responses to dy- acclimatized). namic exercise are predictable when healthy individu- 5. The answer is B. Fever enhances the body’s defenses, als differing in endurance exercise capacity are com- partly by magnifying the responses of leukocytes and pared at matched levels of relative oxygen transport macrophages to the other stimuli that are operative demand. Exercise at 75% of the maximal oxygen up- during an immune response. Choice E reflects what take will lead to exhaustion in typically 1 to 2 hours, was widely believed until the 1970s. Although a few rendering choice B incorrect. The more highly trained pathogens do not flourish at temperatures above 37C, person will show increased work output despite fatigu- they are so much the exception that A is not the best ing at about the same time as the person with lower ca- choice. pacity, rendering choices C and D incorrect. Training 6. The answer is C. The classic changes observed in heat lowers lactic acid production at any matched fractional acclimatization are lower heart rate during exercise; an use of the maximal oxygen uptake, making choice E in- increased sweating response; and a lower core tempera- correct. ture during exercise, which is due to both the increased 3. The answer is D. Active muscle vasodilation during dy- sweating response and a lower thermoregulatory set namic exercise is quantitatively much greater than the net vasoconstriction in the gut, skin, kidneys, and in- point. In addition, salt is conserved by a reduced salt active muscle. Choices B, C, and D contradict this an- concentration in sweat. swer. Total systemic vascular resistance can be meas- 7. The answer is B. Before the hike, the total osmotic con- ured, albeit indirectly, from measurements of systemic tent of the body was 40 L
280 mosm/L  11,200 arterial pressure and cardiac output. mosm (assuming that plasma osmolarity  2
plasma 4. The answer is C. This answer presumes that vasocon- [Na ]). The subject lost 400 mmol (50 mmol/L
8 L) striction occurs in these vascular beds and that its ef- of NaCl or 800 mosm from the ECF in sweat and re- fect is to help balance vasodilation in active skeletal placed all of his water losses. His plasma osmolarity af- muscles and prevent exercise-induced systemic hy- ter the hike and rest is 260 mosm/L [(11,200  800 potension. This effect is ubiquitous across all individu- mosm)  40 L], or plasma [Na ]  130 mmol/L. The als during all forms of dynamic exercise, making reduced plasma osmolality causes water to move from choices B, C, and E incorrect. Cerebral blood flow is the ECF into the cells until a new osmotic equilibrium held constant during all forms of exercise, unlike renal is established. The initial Na content of the subject’s or splanchnic blood flow. ECF was 15 L
140 mmol/L  2,100 mmol. He lost 5. The answer is A. Even highly trained and heat-accli- 400 mmol Na during the hike, and his ECF [Na ] was matized individuals are at risk for heat-related illness if lowered to 130 mmol/L. His new ECF volume  exercise is sufficiently prolonged and if environmental (2,100  400 mmol)  130 mmol/L  13.1 L. conditions are sufficiently severe. In healthy persons 8. The answer is B. His metabolic rate is 800 W; however, during exercise, coronary vasodilatory capacity is ade- he is performing external work at a rate of 140 W and quate, renal blood flow reductions in health are en- needs to dissipate 660 W ( 800 W  140 W) as heat. tirely safe, and gastric mucosal blood flow reductions (It is true that he requires a higher metabolic rate to go are easily tolerated. In long-term exercise in a warm en- uphill than if he were going on a level road, but we vironment, hypotension, not hypertension, is the pos- have already specified his metabolic rate.) His skin sible cardiovascular risk. temperature is 14C above air temperature, and the 6. The answer is E. During dynamic exercise, the balance 2 convective heat transfer coefficient is 15 W/(m C), of active muscle vasodilation and sympathetically 2 so he loses heat by convection at a rate of 210 W/m of driven vasoconstriction in other organs provides the 2 surface area. Because his body surface area is 1.8 m , highest systemic arterial pressure when the involved convection accounts for a loss of 378 W, leaving 282 muscle mass size is intermediate. Isometric exercise al- W  16,920 J/min to be dissipated by evaporation of ways causes blood pressure to increase more than sweat. Because it takes evaporation of 1 g of sweat to matched dynamic exercise. Prolongation of work low-

APPENDIX A Answers to Review Questions 729 ers blood pressure. The state of training, fatigue, and rest and recovery for activated cells, delaying fatigue. prolongation of activity are largely irrelevant or non- Inactive muscle cells undergo atrophic changes that re- specific as factors affecting blood pressure during exer- duce cell cross-sectional area, reducing strength and cise. increasing the number of mobilized cells and motor 7. The answer is E. The baroreceptor blood pressure set units required for a fixed external force development. point is increased during exercise, depending on exer- These facts contradict choice A. Atrophy causes all cise mode, intensity, and duration. Blood pressure only systems required for force production to down-regu- falls during exercise when there is preexisting cardiac late in parallel, contradicting choice B, and lack of ac- disease or during prolonged work in the heat. Training tivity reduces, rather than increases, oxidative capac- has no apparent effects on the baroreflex. ity, rendering choice D erroneous. Choice E is false 8. The answer is E. In the broadest terms, the changes in because the form of exercise must be standardized for cholesterol transport in response to chronically in- meaningful comparisons of strength or endurance. creased physical activity occur from prolonged en- 14. The answer is E. Relative to weight-bearing activity, hancement of fat metabolism. The increase in HDL estrogen plays a more important role in the mainte- and decrease in LDL occur, at least in part, in response nance of bone mass in women. Reductions in bone to enhanced lipoprotein lipase activity and increased mass, which increase the risk of fracture and are invari- apo A-I synthesis. These effects of long-term, regular, ably associated with reduced body weight, occur de- dynamic exercise are largely independent of diet and spite increased dynamic exercise endurance and intra- weight loss. muscular adaptations that are appropriate for the high 9. The answer is B. A normal or reduced arterial PCO 2 is level of dynamic exercise training. a respiratory response that regulates arterial blood pH 15. The answer is D. Increases in both insulin-dependent during exercise. Oxygen partial pressure significantly and insulin-independent glucose uptake in active mus- declines in arterial blood during exercise only when cles during exercise enhance the measured insulin sen- there is preexisting lung disease (choice A), while the sitivity. These effects reduce the requirements for ei- respiratory control system allows ventilation to match, ther insulin itself or for oral antiglycemic agents in but not exceed, levels of CO 2 production (choice C). persons with type 2 diabetes. In contrast, in type 1 di- Exercise in healthy persons does not result in respira- abetes, these same effects increase the risk for hypo- tory acidosis or dizziness resulting from decreased glycemia, leading to requirements for careful monitor- cerebral perfusion. ing of activity, as well as food intake, insulin 10. The answer is B. Exercise training has no effect on lung administration, and stress in persons with this illness. tissues other than the respiratory muscles. The incor- All of the other choices directly contradict this princi- rect choices represent aspects of lung function that are ple, other than choice B, which is incorrect because in- determined by lung tissues unaltered by any form of creased sympathetic activity during exercise directly physical activity. Decreases in ventilation and dyspnea reduces pancreatic insulin release and blood insulin during exercise do occur with chronic increases in dy- levels. namic exercise, but these arise from adaptations local- 16. The answer is C. Maternal activity reduces the risk of ized in the active skeletal muscles (including the respi- maternal gestational diabetes as a result of the same ratory muscles). mechanisms (increased insulin-dependent and insulin- 11. The answer is D. Weight-bearing exercise and in- independent muscle glucose uptake) that reduce the creased muscle strength reduce osteoporosis by in- risk and severity of type 2 diabetes in all persons. There creasing the forces applied to bone. These changes are are no known negative effects of maternal exercise on augmented by exercise-linked improvements in motor either the course or pregnancy or its outcome, and ma- coordination that reduce the risk of falls. These factors ternal exercise does not alter the duration of gestation in combination sharply reduce the incidence of hip or fetal weight at term. fracture in older persons. Activities that decrease grav- itational forces on bone (e.g., water immersion), while Chapter 31 valuable, decrease forces applied to bone and are less useful in the prevention of osteoporosis. 1. The answer is C. Right or left shifts in dose-response 12. The answer is D. Eccentric contractions cause delayed curves indicate changes in sensitivity. Changes in max- muscle soreness. This muscle inflammatory response is imal biological response indicate changes in respon- a result of the greater force per active motor unit found siveness. Because there is no change in maximal re- during eccentric as compared with concentric exercise sponse, the correct answer must relate to a change in at the same force development. Soreness is not found sensitivity only. A right shift indicates decreased sensi- after isometric exercise (choice A), solely on the basis tivity. of ischemia (which occurs in many forms of muscle 2. The answer is C. Hormones produce their effects on contraction; choice B), in response to increased en- target cells by interacting with specific receptors. Hor- durance (choice C), or in direct proportion to the per- mone binding to its receptor generally initiates a cas- centage usage of the maximum voluntary contractile cade of events that lead to biological effects in the tar- force (which is defined in terms of isometric contrac- get cells. tions; choice E). 3. The answer is A. Aldosterone is a steroid and the pri- 13. The answer is C. Motor unit rotation allows frequent mary mineralocorticoid in the body. Testosterone,

730 APPENDICES progesterone, and cortisol are steroid hormones hav- 6 months postpartum in a nonnursing mother. The ing primarily androgen, progestin, and glucocorticoid combination of both galactorrhea and amenorrhea is activities, respectively. Prostaglandin E 2 is a local sig- diagnostic of a PRL-secreting pituitary tumor. TSH naling molecule derived from arachidonic acid. generally has little effect on PRL secretion. GH has 4. The answer is B. Scatchard plots of hormone-receptor lactogenic activity when high, not low. Hypothalamic binding data give information regarding the number of dopamine is an inhibitor of PRL release. receptors and the affinity of the hormone for its recep- 4. The answer is A. Neurophysin is the other product tor. The x-intercept provides data regarding total re- generated when the prohormone for AVP or oxytocin ceptor number, and the slope is equal to the negative is cleaved. A decrease in blood volume would result in of the association constant (K a ). the release of AVP and neurophysin from magnocellu- 5. The answer is D. Preprohormones are the gene prod- lar neurons. The hormones oxytocin, -lipotropin, ucts for most peptide and protein hormones. These are ACTH, and somatostatin are not involved in the regu- rapidly cleaved to form prohormones. POMC and pro- lation of blood volume. pressophysin are two examples of specific prohor- 5. The answer is C. Growth hormone deficiency in adults mones. is characterized by decreased muscle strength and ex- 6. The answer is E. Cortisol, like other steroid hormones, ercise intolerance and a reduced sense of well-being is carried in the blood largely bound to carrier proteins, (including effects on libido). Lean body mass (muscle) although a small percentage exists free in solution. The is lost, and excess body fat deposition occurs in the ab- majority of cortisol is bound to a specific carrier pro- dominal region. GH replacement can reverse these ef- tein, corticosteroid-binding globulin (CBG), while fects. Thyroid dysfunction is ruled out by the normal smaller amounts are bound nonspecifically to albumin. thyroid hormone levels. Glucocorticoid deficiency Few, if any, cortisol receptors would be expected in the usually results from primary adrenal insufficiency, as in plasma and transthyretin binds primarily thyroxine. Addison’s disease. Clinical symptoms include a de- 7. The answer is D. Hormones generally circulate at con- creased sense of well-being, GI disturbances, and ab- centrations from 10 9 to 10 12 M. They produce normal glucose metabolism. Primary adrenal insuffi- much larger changes in a variety of biological parame- ciency is also characterized by high blood levels of ters as a result of signal amplification, in which the ACTH, which can result in hyperpigmentation as a re- rather weak hormonal signal is amplified into a larger sult of the melanocyte-stimulating activity of the biological response. amino terminal portion of ACTH. Adrenal insuffi- ciency is not usually associated with a redistribution of body fat to central stores. Prolactin does not appear to Chapter 32 have a major physiological effect in human males. 1. The answer is C. Destruction of the neurons in the par- Acromegaly results from excessive GH secretion in an aventricular nuclei of the hypothalamus decreases adult; the symptoms are not consistent with CRH release, which causes decreased synthesis and se- acromegaly. cretion of ACTH. Hyperosmolality of the blood 6. The answer is C. The data demonstrate a higher aver- would lead to an increase in portal blood AVP, which age ACTH and higher average cortisol concentration increases ACTH secretion by corticotrophs. Physical in the evening hours. This is opposite the usual diurnal or emotional stress increases ACTH release. Glucocor- pattern in which ACTH and cortisol are high in the ticoids feed back to the hypothalamus and anterior pi- morning. It is possible that the subject works nights tuitary to decrease ACTH synthesis and secretion. Pri- and has a reversed but normal diurnal rhythm of mary adrenal insufficiency is characterized by a lack of ACTH and cortisol release. There is no adrenal disease glucocorticoids in the blood, resulting in an increase in (primary or secondary) because both ACTH and cor- ACTH synthesis and secretion. Increased PKA activity tisol are higher at the same time and then are lower at in corticotrophs increases ACTH synthesis and secre- the same time. The diurnal pattern rules out an ACTH- tion. secreting tumor because ACTH release would tend to 2. The answer is D. Thyroid hormones stimulate the ex- be constant. pression of the GH gene in somatotrophs. Thyroid 7. The answer is B. Somatostatin, given as a long-acting hormones exert a negative-feedback signal on the hy- analog octreotide, is effective in reducing excess secre- pothalamic-pituitary-thyroid axis to inhibit their own tion of GH. It can also reduce tumor size, if one is pres- synthesis and secretion. Therefore, thyroid hormones ent. Glucocorticoid would feed back to inhibit the hy- decrease the sensitivity of thyrotrophs to TRH, decrease pothalamic-pituitary-adrenal axis but have little effect the formation of IP 3 in thyrotrophs, inhibit the expres- on GH release. Because acromegaly is characterized by sion of the genes for the
and  subunits of TSH in excessive GH secretion, the administration of GH thyrotrophs, and decrease the secretion of TSH by thy- would be inappropriate. Insulin could be given to rotrophs. Thyroid hormones have no effect on ACTH counter the diabetogenic effects of excess GH, but it release. would have little effect on tumor size (if present), bone 3. The answer is B. Galactorrhea is commonly associated thickening, or hypertrophy of the liver. GHRH and with pituitary tumors secreting excess PRL. Prolactin is thyroid hormone would stimulate GH release in a situ- important in maintaining breast milk production after ation of high GH. birth. Galactorrhea is diagnosed if present longer than 8. The answer is B. GHRH increases cAMP and stimu-

APPENDIX A Answers to Review Questions 731 lates GH synthesis and secretion; somatostatin de- because of the protective actions of the thyroid hor- creases cAMP and inhibits GH synthesis and secretion mone-binding proteins. Thyroid peroxidase catalyzes from somatotrophs. TRH stimulates TSH secretion the iodination of thyroglobulin to form MIT and DIT, and the synthesis of the
and  subunits of TSH by precursor molecules for T 3 . increasing inositol trisphosphate and calcium in thy- 6. The answer is D. The patient’s symptoms of chronic fa- rotrophs. cAMP has no effect on AVP release, and it tigue, aching muscles, occasional numbness in the fin- stimulates ACTH synthesis in corticotrophs. gers, and weight gain are consistent with a hypothy- roid state. The high TSH rules out a defect in the Chapter 33 hypothalamic-pituitary axis and suggests an unrespon- sive thyroid gland, most likely a result of autoimmune 1. The answer is A. TSH stimulates the endocytosis of thyroid disease. The presence of antibodies to thyroid colloid by the apical membrane of the follicular cell. peroxidase or thyroglobulin would confirm the diag- Thyroglobulin in the colloid is hydrolyzed in the lyso- nosis. The absence of a goiter rules out hypothy- somal vesicles to release thyroid hormones. T 4 and T 3 roidism as a result of iodine deficiency; low serum thy- are stored in thyroglobulin in the colloid, not in secre- roid hormone levels would result in elevated TSH with tory vesicles in the follicular cell. TSH stimulates the subsequent trophic effects on thyroid growth. There is uptake of iodide from the blood, not the colloid. It has no growth of the thyroid in this patient because of the no effect on blood flow to the thyroid gland and no di- autoimmune attack on the gland. rect effect on the binding of T 4 and T 3 to thyroxine- 7. The answer is B. Thyroid peroxidase catalyzes the cou- binding globulin. TSH stimulates an increase in cAMP, pling of two adjacent iodotyrosine residues in the thy- not an increase in the hydrolysis of this second mes- roglobulin precursor to form iodothyronine and dehy- senger. droalanine. Thyroid peroxidase uses hydrogen 2. The answer is C. Thyroid hormones are important for peroxide produced by mitochondria to iodinate tyro- normal development of the CNS and for body growth. sine residues and to couple adjacent iodotyrosine TSH stimulates the synthesis and release of thyroid residues. Thyroid peroxidase is localized to the apical hormones, as well as the growth of the thyroid gland. membrane of the follicular cell and catalyzes all reac- In a disorder in which the thyroid gland does not re- tions in this location. The release of thyroid hormone spond to TSH, thyroid hormone production would be is mediated by lysosomal degradation of thyroglobu- decreased, resulting in poor development of the CNS lin. Thyroid peroxidase iodinates tyrosine residues in and poor body growth. TSH would also not be able to the thyroglobulin molecule to form MIT and DIT. De- stimulate the growth of the thyroid, resulting in a small hydroalanine is derived from the free-radical re- gland. arrangement of 2 DIT residues to form thyroxine. Thy- 3. The answer is A. Giving thyroid hormones to the child roid peroxidase forms the free radicals necessary for would improve body growth but not mental ability be- this reaction. cause thyroid hormones are most important for CNS 8. The answer is F. A TSH secreting tumor of the pitu- development in utero. Therefore, giving thyroid hor- itary would result in elevated thyroid hormone levels mones after birth would be too late. Thyroid gland size and symptoms of thyrotoxicosis. Graves’ disease is would remain smaller than normal because thyroid characterized by elevated thyroid hormone levels and hormones have no trophic effect on the gland; only anti-TSH receptor antibodies. TSH would be low be- TSH has a trophic effect. cause of feedback inhibition of its release. Resistance 4. The answer is C. Uncoupling proteins allow protons to to thyroid hormone action could result in elevated thy- flow down their electrochemical gradient across the roid hormone levels but would not cause symptoms of mitochondrial membrane, uncoupled from the synthe- thyrotoxicosis. Thyroid gland adenomas commonly sis of ATP. The resulting energy generated is released result from a point mutation in the TSH receptor, re- as heat, and ATP is not synthesized. Uncoupling pro- sulting in chronic activation of signaling. This would teins are increased by thyroid hormones. The novel increase thyroid hormones but should result in a re- uncoupling proteins are found in many tissues, includ- duction in TSH. A deficiency in 5-deiodinase could ing muscle and adipose tissue. Oxidation of fatty acids result in increased thyroid hormone levels and symp- and glucose is not coupled in mitochondria, and the toms of thyrotoxicosis, but would not be associated uncoupling proteins are not the switch between oxida- with elevated TSH. Early in the progression of tion of these two substrates. Uncoupling proteins have Hashimoto’s disease, symptoms of thyrotoxicosis may not been demonstrated to be essential to the mainte- be present, but the absence of antithyroid antibodies nance of body temperature in mammals. However, rules out this condition. UCP-1 is important in the ability of small mammals, such as rodents, to tolerate cold temperatures. Chapter 34 5. The answer is F. T 3 is produced from T 4 by 5-deiodi- nase (type 2) in the anterior pituitary. The major thy- 1. The answer is B. Cholesterol esters in LDL are the roid hormone product of the thyroid gland is T 4 . The most important source of cholesterol for sustaining ad- thyroid hormone receptor (TR) is located in the nu- renal steroidogenesis when it occurs at a high rate over cleus. A 5-deiodinase acts on T 4 to make reverse T 3. a long time. This cholesterol can be used directly after The half-life of T 3 in the bloodstream is about 1 day release from LDL and not stored. De novo synthesis of

732 APPENDICES cholesterol from acetate is a minor source of choles- 6. The answer is F. IP 3 is one of the second messengers in terol in humans. Cholesterol from the plasma mem- the cells of the zona glomerulosa that signals for al- brane or endoplasmic reticulum is not used for dosterone release. A decrease in IP 3 would result in less steroidogenesis. Cholesterol esters in lipid droplets signal for aldosterone synthesis and release. The rate of within adrenal cortical cells would be used first and de- aldosterone secretion would increase in response to an pleted during periods of high adrenal steroid hormone increase in renin release from the kidney. Renin cat- synthesis. alyzes the rate-limiting step in the conversion of an- 2. The answer is C. The increase in body weight with lit- giotensinogen to angiotensin II, which is a stimulus for tle linear growth suggests that the patient has Cush- aldosterone synthesis and release. A rise in serum ing’s disease rather than general obesity because linear potassium or renal sympathetic nerve activity, a fall in growth usually continues in obesity syndromes. Labo- blood pressure in the kidney, or a decrease in tubule ratory findings in Cushing’s disease include elevated fluid sodium concentration at the macula densa would ACTH, serum cortisol, urinary cortisol, and serum in- stimulate aldosterone synthesis and release. sulin (as a result of the cortisol-induced resistance to 7. The answer is C. The first and rate-limiting step in all insulin action in skeletal muscle and adipose tissue). steroid biosynthesis is catalyzed by cholesterol side- 3. The answer is A. Congenital adrenal hyperplasia is the chain cleavage enzyme, resulting in pregnenolone and result of genetic defects that affect adrenal steroido- isocaproic acid. 17
-hydroxylase, 3-hydroxysteroid genic enzymes, producing an impaired formation of dehydrogenase, 21-hydroxylase, and 11-hydroxylase cortisol. Low serum cortisol is a stimulus for ACTH re- are all involved in the synthesis of cortisol, but are not lease from the hypothalamus. The increase in ACTH rate-limiting. 3-Hydroxy-3-methylglutaryl CoA re- has a proliferative effect on the adrenal gland, resulting ductase catalyzes the rate-limiting step in de novo cho- in hyperplasia. Addison’s disease is the result of patho- lesterol synthesis. logical destruction of the adrenal glands by microor- 8. The answer is B. Addison’s disease results from the ganisms or autoimmune disease and would, therefore, pathological destruction of the adrenal glands by mi- not result in adrenal hyperplasia. ACTH stimulates the croorganisms or by an autoimmune response; it is char- growth of the adrenal gland. A reduction in ACTH in acterized by glucocorticoid and aldosterone deficiency. the blood would result in atrophy of the adrenal gland. Hyperpigmentation is caused by a lack of cortisol pro- Corticosteroid-binding globulin noncovalently binds duction, which results in increased ACTH production. steroid hormones in plasma; defects in this protein are Hyponatremia and hyperkalemia occur in the absence not associated with adrenal hyperplasia. Cushing’s dis- of aldosterone, which normally stimulates sodium re- ease results from a pituitary ACTH-secreting tumor; tention and potassium excretion by the kidneys. Cush- adrenal hyperplasia is secondary, not congenital, in ing’s disease produces excessive cortisol release from this disease. Aldosterone synthesis is regulated by the the adrenals, secondary to excessive anterior pituitary renin-angiotensin system. Defective aldosterone syn- secretion of ACTH; patients with this disease do not thesis would, therefore, not lead to increased ACTH have the symptoms of aldosterone deficiency. Primary and adrenal hyperplasia. hypoaldosteronism is characterized by a lack of aldos- 4. The answer is E. Catecholamines stimulate terone secretion. The hyperpigmentation indicates a glycogenolysis and gluconeogenesis in the liver, caus- more severe disease with lack of cortisol production as ing glucose to be synthesized and released into the well. Congenital adrenal hyperplasia is the result of ge- blood. Catecholamines stimulate glycogen phospho- netic defects that affect adrenal steroidogenic enzymes, rylase in muscle to free glucose for use by the muscle. resulting in impaired formation of cortisol. Low serum Muscle cannot release glucose to the circulation be- cortisol is a stimulus for ACTH release and hyperpig- cause it lacks glucose-6-phosphatase. However, the mentation. Congenital adrenal hyperplasia is usually as- muscle can release lactate, which can be used in gluco- sociated with hypertension as a result of the excess pro- neogenesis by the liver. Catecholamines inhibit the re- duction of steroidogenic intermediates such as lease of insulin from the pancreas. Insulin would be deoxycorticosterone, which has substantial mineralo- counterproductive to attempts to increase blood glu- corticoid activity. Hypopituitarism is a condition in cose. Catecholamines increase the release of fatty acids which pituitary function is suppressed, resulting in re- from the adipose tissue, to be used in gluconeogenesis duced ACTH secretion; this is not applicable because by the liver. the patient presents with hyperpigmentation as a result 5. The answer is F. Patients on long-term glucocorticoid of excess ACTH release. Patients with glucocorticoid- therapy should have the dose increased prior to under- suppressible hyperaldosteronism are hypertensive. going surgery to minimize the effects of surgical stress. 9. The answer is E. Glucocorticoids maintain the tran- These patients cannot mount their own stress response scription of genes and, therefore, the intracellular con- because of the lack of adrenal cortisol release. Gluco- centrations of many of the enzymes needed to carry corticoid-induced hypoglycemia or interactions with out gluconeogenesis in the liver and kidneys. Gluco- anesthetics are unlikely, and these concerns would be corticoids maintain the liver and kidneys in a state that secondary to stimulating the response to surgical makes them capable of accelerated gluconeogenesis stress. Glucocorticoids inhibit ACTH release and the when fasting occurs. Glucocorticoids inhibit insulin re- immune response. Glucocorticoids increase the re- lease. Insulin inhibits gluconeogenic enzymes in the sponse of the vasculature to catecholamines. liver. The glucocorticoid-induced inhibition of glu-

APPENDIX A Answers to Review Questions 733 cose utilization by skeletal muscle does not stimulate cholecalciferol in the skin. Vitamin D 3 is not converted gluconeogenesis but provides glucose for utilization by to vitamin D 2 . Calcium is incorporated into hydroxya- the CNS. Inhibition of glycogenolysis by glucocorti- patite in bone. coids does not occur in fasting. Glucocorticoids do not 6. The answer is C. Osteoporosis is characterized by an inhibit, but actually permit, lipolysis and the release of equivalent loss of bone mineral and organic matrix. fatty acids from adipose tissue. Paget’s disease is characterized by disordered bone re- modeling; rickets and osteomalacia are characterized Chapter 35 by inadequate bone mineralization. 7. The answer is D. PTH stimulates bone resorption and 1. The answer is D. Epinephrine stimulates glucagon se- renal calcium reabsorption and, via stimulated synthe- cretion but inhibits insulin secretion. Amino acids and sis of 1,25-dihydroxycholecalciferol, intestinal calcium acetylcholine both stimulate insulin and glucagon se- absorption, raising plasma calcium concentration. cretion. PTH inhibits renal phosphate reabsorption, leading to 2. The answer is C. Insulin inhibits protein degradation phosphaturia and hypophosphatemia. and stimulates amino acid uptake in skeletal muscle. It stimulates glucose uptake in many, but not all, tissues. Chapter 37 It inhibits hormone-sensitive lipase in adipose tissue. 3. The answer is C. Glucagon stimulates gluconeogene- 1. The answer is A. Reduced secretion of GnRH will re- sis and ureagenesis in the liver. Under certain condi- sult in extremely low levels of circulating LH and FSH, tions, glucagon can actually stimulate insulin secretion. causing testicular atrophy, as in Kallmann’s syndrome. Glucagon does not have its primary actions in adipose Hypersecretion of LH and FSH, increased activin, and tissue. Somatostatin does not play a role in ketogene- an increased number of FSH receptors all lead to hy- sis. perfunction of the testis, not hypofunction. A failure of 4. The answer is B. Persons with type 1 diabetes are in- the hypothalamus to respond to testosterone increases sulin-deficient, not insulin resistant; they are treated LH, leading to increased Leydig cell androgens and with exogenous insulin. Persons with type 2 diabetes testicular hypertrophy. are treated with sulfonylureas. Secondary complica- 2. The answer is E. Follistatin is a binding protein for ac- tions are difficult to avoid in any form of diabetes. tivin. Activin cannot increase FSH secretion when fol- 5. The answer is A. The development of type 2 diabetes listatin is bound to it, so FSH secretion decreases. Fol- has a strong genetic component. Persons with type 2 listatin does not bind FSH, does not inhibit seminal diabetes often have normal or elevated insulin levels. fluid production and Leydig cell testosterone secretion, Although there is an association of type 2 diabetes and and does not stimulate the production of spermatogo- obesity, it is not true that it only occurs in obese indi- nia. viduals. Type 1 diabetes is a disease of insulin defi- 3. The answer is A. The epididymis and vas deferens are ciency, and type 2 is a disease of insulin resistance. major storage sites of spermatozoa. Spermatozoa de- 6. The answer is D. Neuropathy, nephropathy, and velop in the in the seminiferous tubules. Sertoli cells, retinopathy are chronic complications of type 2 dia- not the epididymis, secrete estrogens and inhibin. The betes. Ketoacidosis is an acute complication seen in prostate gland, seminal vesicles, and bulbourethral type 1 diabetes. glands secrete the seminal fluids. 7. The answer is D. Delta cells produce somatostatin. 4. The answer is B. It takes approximately 65 to 70 days 8. The answer is D. The I/G ratio is highest after feeding to develop spermatozoa from the earliest stages of and decreases progressively during fasting. spermatogonia. Because the production of sperm de- pends on LH and FSH, a lack of GnRH (Kallmann’s Chapter 36 syndrome) will reduce the production of LH, FSH, and sperm. Temperature is important in regulating sperm 1. The answer is B. Half (50%) of the total plasma cal- production. Optimal sperm production occurs at 2 to cium is free or ionized. 3C lower than body temperature. 2. The answer is C. Most of the ingested calcium is not 5. The answer is A. The initial reaction and the rate-lim- absorbed by the GI tract and leaves the body via the fe- iting step in the production of testosterone is the con- ces. version of cholesterol to pregnenolone, which is regu- 3. The answer is A. The majority of ingested phosphate lated by is absorbed by the GI tract and leaves the body via the 6. The answer is LH-stimulated cAMP in the Leydig cells. urine. The cholesterol side-chain cleavage enzyme is located 4. The answer is A. Skin, kidney, and liver can all be in- in mitochondria. All other sex hormone synthesis oc- volved in forming the active metabolite of vitamin D, curs outside of the mitochondria. Aromatization is the 1,25-dihydroxycholecalciferol. Bone does not form last reaction, the conversion of testosterone to estra- this hormone, but is a target for its actions. diol. Pregnenolone is the immediate derivative of cho- 5. The answer is C. The kidneys are the site of formation lesterol, not progesterone. The initial reaction is stim- of 1,25-dihydroxycholecalciferol from 25-hydroxyc- ulated by LH, not FSH. LH receptors are on Leydig holecalciferol, a reaction catalyzed by the 1
-hydrox- cells, the site of testosterone synthesis. ylase enzyme. 7-Dehydrocholesterol is converted to 7. The answer is C. The enzyme 5
-reductase is found in

734 APPENDICES the prostate and converts testosterone to dihy- zyme called 17
-hydroxylase, which converts proges- drotestosterone. Testosterone does not bind HDL; terone to 17-hydroxyprogesterone. Aromatase is the HDL is a source of cholesterol. Activin does not bind enzyme that converts androgens to estrogens. 5
-Re- testosterone. Testosterone cannot be converted di- ductase converts testosterone to dihydrotestosterone. rectly to 17-hydroxyprogesterone, which is derived Sulfatase is an enzyme that conjugates steroids with from progesterone and is converted to androstene- sulfate for subsequent excretion in the urine. Steroido- dione. The side-chain cleavage enzyme converts cho- genic acute regulatory protein transports cholesterol lesterol to pregnenolone. from the outer to the inner mitochondrial membrane. 8. The answer is A. Sex hormone-binding globulin binds 3. The answer is B. One of the first clinical measures for to both testosterone and estradiol, but it binds with menopause is an increase in the serum concentration of higher affinity to testosterone. The bioactivity of FSH (and LH), indicative of the lack of ovarian func- testosterone is reduced by SHBG because testosterone tion. Menses starts at age 12, not age 50, and its onset cannot bind to its receptor when bound by SHBG. at this time would not indicate menopause. Excessive SHBG increases the circulating half-life of testosterone corpora lutea would likely indicate multiple ovulations by slowing the clearance and metabolism of testos- or a failure of luteal regression. Increased vaginal corni- terone. SHBG does not alter the secretion of inhibin or fication is an indicator of estrogen secretion, which androgen-binding protein. does not occur in menopause. Menstrual cycles be- 9. The answer is D. The production of estradiol requires come irregular at menopause. Leydig cells, under the influence of LH, which stimu- 4. The answer is D. Progesterone has a thermogenic ef- lates androgen production. The androgen diffuses to fect on the hypothalamus, increasing the basal body Sertoli cells, which contain aromatase, the enzyme temperature for a few days after ovulation. Women that converts androgens to estrogens under the influ- who, because of ovulatory problems, are having trou- ence of FSH. Therefore, Leydig cells, Sertoli cells, LH, ble getting pregnant are sometimes asked to record and FSH are required. Follistatin binds activin and their daily oral temperatures and look for the increase would reduce FSH secretion, an essential component in basal body temperature, indicating an increase in for estradiol production. Estradiol is not produced by progesterone (which indicates ovulation). Proges- Leydig cells. Activin would increase the secretion of terone induces a secretory type of endometrium, FSH, which is a necessary component for estradiol, but whereas estrogens induce a proliferative type. During other cells and hormones are required. Similarly, Ley- the luteal phase, when progesterone is increasing, dig cells would need LH to stimulate the production of graafian follicles are not present. Progesterone levels the androgen precursor of estrogen. Sertoli cells, under decrease during luteal regression. FSH decreases when the influence of FSH, are needed to aromatize andro- progesterone is rising. gen from Leydig cells. 5. The answer is A. Theca interna cells produce andro- 10. The answer is C. Androgens and estrogens are known gens under the influence of LH, whereas granulosa to stimulate the closure of the epiphyses at puberty. cells do not produce androgens. Theca interna cells do Because eunuchs are castrated, they have no testicular contain cholesterol side-chain cleavage enzyme, source of androgen and estrogen, and the closure of which converts cholesterol to pregnenolone. Because the epiphyses is delayed. In eunuchs, long bones con- theca cells do not express aromatase, they cannot con- tinue to grow, resulting in a tall stature. Estrogens do vert testosterone to estradiol. The theca interna has a have a positive effect in maintaining bone; however, rich blood supply. Granulosa cells produce inhibin. eunuchs have little or no estrogen because the testes 6. The answer is A. Disruption of the hypothalamic-pitu- are absent. Choice B is incorrect, although eunuchs itary portal system leads to a lack of dopamine and may have elevated circulating LH (as a result of the GnRH reaching the pituitary. Because dopamine in- lack of androgen negative feedback). LH has no effect hibits PRL secretion, PRL levels will increase. In addi- on bone. The absence of testes delays the closure of tion, the lack of GnRH will lead to reduced secretion the epiphyses, and androgen levels are low in eunuchs of LH and FSH, reduced ovarian function, and even- because of the lack of testes. tual ovarian atrophy. PRL will have no effect on the ovary or inhibit ovarian follicle development. Disrup- Chapter 38 tion of the hypothalamic-pituitary axis will lead to re- duced follicular development, lack of ovulation, and 1. The answer is B. Aromatase is present only in granu- low circulating progesterone. Inhibin levels will de- losa cells and is regulated mainly by FSH. Although crease, but FSH will not increase because there is no LH may stimulate aromatase in granulosa cells, granu- GnRH reaching the pituitary from the disrupted axis. losa cells do not produce androgens. Estradiol synthe- Excessive ovarian androgen usually occurs in the pres- sis in the graafian follicle is unrelated to progesterone ence of excessive LH secretion or an androgen tumor synthesis in the corpus luteum and does not increase in the ovary. LH secretion is reduced by the lack of LH during this phase. Estradiol increases LH secretion GnRH. during the LH surge. There is no evidence for synergy 7. The answer is B. Inhibin is produced by granulosa cells between FSH and progesterone in regulating estradiol and inhibits the secretion of FSH. Inhibin does not in- secretion by the graafian follicle. hibit the secretion of LH and PRL. Although inhibin 2. The answer is A. Granulosa cells do not have the en- can have local ovarian effects, it has profound in-

APPENDIX A Answers to Review Questions 735 hibitory effects on FSH secretion. Inhibin has two reaction and pronuclei formation occur after the sperm forms, A and B; the
subunits are the same, whereas has entered the ovum. Sperm enter the perivitelline the  subunits are different. Inhibin binds activin and space after penetration; there is no evidence that this decreases FSH secretion. space has any role in penetration. Cumulus expansion 8. The answer is D. Estrogen induces the formation of a assists in movement of the sperm through the mass of stringy vaginal secretion that is called spinnbarkeit, granulosa cells for the sperm to get to the surface of the observed in the late follicular phase. The secretory en- zona pellucida. However, the cumulus cells do not as- dometrium is under the influence of progesterone; sist in actual penetration of the zona. therefore, spinnbarkeit would not be present. 4. The answer is B. The production of hCG by tro- Spinnbarkeit is not produced in response to proges- phoblast cells stimulates the corpus luteum to continue terone, androgen, or prolactin. to produce progesterone so that luteal regression does 9. The answer is A. Fertilization occurs in the oviduct. not occur at the end of the anticipated cycle. Although The oocyte must have entered a second meiotic divi- PRL levels increase throughout pregnancy, PRL is not sion to reduce the chromosome number of the oocyte responsible for maintenance of the corpus luteum of to a haploid state (n) so that it may fuse with the sperm pregnancy. Prostaglandins are generally luteolytic, (also haploid), producing a 2n zygote. Fertilization causing regression of the corpus luteum, termination of does not occur in the uterus, especially not after the the luteal phase, and return to the next cycle; they do first meiotic division when the chromosome number is not prolong the cycle or postpone it. Oocytes are not 2n. In the adult ovary, oocytes do not undergo mitosis. depleted after implantation. In fact, pregnancy tends Graafian follicles do not enter the oviduct and are not to preserve oocytes, as ovulation ceases during preg- fertilized. Fertilization does not occur in the uterus, nancy. Plasma progesterone levels are high during and the oocyte does not implant. The blastocyst will pregnancy as a result of activation of the corpus luteum implant in the uterus. In addition, extrusion of the po- and placental production of progesterone. Elevated lar body is associated with fertilization, but this event progesterone blocks follicular development and the occurs within the oviduct. ensuing LH surge; low levels of progesterone would 10. The answer is B. 5
-Reductase is the enzyme that con- permit a return to cyclicity. verts testosterone to dihydrotestosterone. 5
-Reduc- 5. The answer is A. Fertilization by more than one sperm tase is associated with increasing the most potent an- is prevented by the cortical reaction. Cortical granules drogen, dihydrotestosterone, and reducing LH containing proteolytic enzymes fuse just beneath the secretion. Estrogens are associated with female sec- entire surface of the oolemma. The proteolytic en- ondary sex characteristics, although some androgens zymes are released to the perivitelline space, destroy regulate pubic hair development. the sperm receptors, and harden the zona, preventing other sperm from penetrating the fertilized ovum. En- zyme reaction is a nonspecific term with little meaning Chapter 39 for polyspermy. The acrosome reaction allows the 1. The answer is D. Suckling involves hormonal and neu- sperm to penetrate the zona. The decidual reaction is ronal components, but the hormonal component is ef- an inflammatory-like reaction that occurs simultane- ferent and the neuronal component is afferent. When ously with implantation of the blastocyst into the uter- the baby suckles, neural signals from the nipple travel ine endometrium. via nerves to the spinal cord and up to the brain (affer- 6. The answer is A. Oral steroidal contraceptives gener- ent component), which triggers the release of oxytocin ally contain progesterone and estrogen-like molecules, from the supraoptic nuclei (efferent component). Oxy- which feed back negatively on the hypothalamic-pitu- tocin enters the circulation, enters the breasts, and itary axis and reduce the secretion of LH and FSH; this causes contraction of the myoepithelial cells. Placental is the primary mechanism of action in preventing preg- lactogen is no longer present after parturition; it is a nancy. Choices B, C, and D are not the best answers, placental hormone. Dopamine release is decreased by although oral contraceptives do alter the uterine envi- suckling, and as a result, PRL secretion is increased. ronment, thicken the cervical mucus, and reduce sperm 2. The answer is D. Under normal circumstances, the motility. If ovulation were not blocked, the other pa- uterus must be primed with both progesterone and es- rameters would not be effective in blocking pregnancy. trogen for successful implantation. Implantation oc- Oral contraceptives block the LH surge; they do not curs on day 7 after fertilization. The decidual reaction induce a premature surge. occurs as the result of the implanting blastocyst. The 7. The answer is D. hCG is produced by trophoblast cells embryo is in the blastocyst stage of development at the prior to implantation of the embryo and binds to luteal time of implantation. A morula does not implant. The LH receptors, signaling them to produce progesterone, developing embryo enters the uterus on day 3 or 4, it which is necessary for the maintenance of pregnancy. remains suspended in the uterus for 3 or 4 more days, Therefore, hCG signals the mother that she is preg- and implantation occurs on day 7. nant via stimulation of luteal LH receptors. Placental 3. The answer is A. The acrosome reaction causes a fusion lactogen is not produced until after pregnancy is well of the plasma membrane and the acrosomal membrane established. Progesterone is a common hormone asso- of the sperm, with subsequent release of proteolytic ciated with the menstrual cycle and pregnancy. In hu- enzymes that help the sperm enter the ovum. The zona mans, the inflammatory reaction at implantation does

736 APPENDICES not signal the mother that she is pregnant and it fol- of insulin resistance. Progesterone, not insulin, in- lows secretion of hCG. creases appetite during pregnancy. 8. The answer is C. The placenta cannot make androgens 10. The answer is C. The female phenotype can develop from progestin precursors because it lacks 17
-hy- in an XY male if the biological action of testosterone is droxylase. DHEAS from the fetal adrenal glands is absent. This absence can be due to a lack of testos- converted to 16OH-DHEAS by the fetal liver and terone secretion caused by enzyme deficiencies or a then to estriol by the placenta; this reaction is substan- lack of the testosterone (DHT) receptor. In this tial and is an indicator of fetal stress (estriol low) or process, called testicular feminization, a phenotypic well-being (estriol high). The mother’s adrenal can female develops in the presence of an XY karyotype. also make DHEAS, which can be converted to 16OH- There is a lack of pubic and axillary hair, well-devel- DHEAS by 16-hydroxylase in the fetal liver, but this oped breasts (as a result of the conversion of testos- reaction is limited (10%). Androgens cannot be pro- terone to estrogen), with inguinal or abdominal testes, duced from cholesterol in the placenta; the placenta no uterus (because AMH is secreted), underdeveloped lacks 17
-hydroxylase. Estradiol is generally not con- male accessory ducts (lack of testosterone action), and verted to estriol. Androgens from the ovary are gener- the vagina ends in a blind pouch. Progesterone has no ally not converted to estriol. effect on phenotype. There is no evidence that adrenal 9. The answer is C. Insulin resistance is associated with insufficiency (low cortisol and androgens from the reduced utilization of glucose by the mother and this adrenals) have any effect on inducing female pheno- glucose is spared for the fetus. Plasma glucose is not type in a male. Inhibin would reduce FSH secretion lower but higher with insulin resistance. Insulin moves and ultimately reduce adult testis size, but in the fetus glucose into cells. During pregnancy, the development there is no effect on the development of the female of insulin resistance may be a predictor of diabetes phenotype. AMH will prevent formation of the later in life. Reduced pituitary function occurs because oviducts, uterus, and upper vagina; it does not increase of the high levels of steroids and PRL, all independent female characteristics in the male.

APPENDIX B Common Abbreviations in Physiology CCK cholecystokinin A amount; area CFC capillary filtration coefficient A alveolar CFTR cystic fibrosis transmembrane conductance a arterial; ambient regulator ABP androgen-binding protein cGMP cyclic guanosine monophosphate (guanosine AC adenylyl cyclase 3
,5
-monophosphate) ACE angiotensin-converting enzyme CGRP calcitonin-gene-related peptide ACh acetylcholine CIA central inspiratory activity AChE acetylcholinesterase CMK calmodulin-dependent protein kinase ACTH adrenocorticotropic hormone (corticotropin) CNS central nervous system ADH antidiuretic hormone CO cardiac output; carbon monoxide ADP adenosine diphosphate COP colloid osmotic pressure (oncotic pressure) AE anion exchanger COPD chronic obstructive pulmonary disease AMH antimüllerian hormone (müllerian-inhibiting COX cyclooxygenase substance) CRH corticotropin-releasing hormone AMP adenosine monophosphate CSF cerebrospinal fluid ANP atrial natriuretic peptide CT computed tomography; calcitonin ANS autonomic nervous system (thyrocalcitonin) AQP aquaporin CYP cytochrome P450 enzyme A r effective radiating surface area D dead space ARDS adult respiratory distress syndrome D diffusion coefficient; diffusing capacity ATP adenosine triphosphate DAG diacylglycerol AV atrioventricular DHEAS dehydroepiandrosterone sulfate A-V arteriovenous DHT dihydrotestosterone AVP arginine vasopressin (antidiuretic hormone or DIT diiodotyrosine ADH) DMT divalent metal transporter aw airway DNA deoxyribonucleic acid B barometric DPG diphosphoglycerate b body; blood DPPC dipalmitoylphosphatidylcholine BF blood flow E extraction (extraction ratio) BMR basal metabolic rate E expiratory BS urinary space of Bowman’s capsule E evaporative heat loss BSC bumetanide-sensitive (Na -K -2Cl ) e emissivity cotransporter EABV effective arterial blood volume BUN blood urea nitrogen ECaC epithelial calcium channel C concentration; compliance; capacitance; ECF extracellular fluid capacity; clearance; kilocalorie; conductance ECG electrocardiogram C heat loss by convection ECL cell enterochromaffin-like cell ccore ED 50 median effective dose CA carbonic anhydrase EDRF endothelium-derived relaxing factor (NO) CaBP calcium-binding protein (calbindin) EDV end-diastolic volume CaM calmodulin EEG electroencephalogram CAM cell adhesion molecule EF ejection fraction cAMP cyclic AMP (cyclic adenosine 3
,5
- EGF epidermal growth factor monophosphate) E ion equilibrium potential for an ionic species CBG corticosteroid-binding globulin EJP excitatory junction potential 737

738 APPENDICES ELISA enzyme-linked immunosorbent assay IC inspiratory capacity membrane potential ICC interstitial cell of Cajal E m ENaC epithelial sodium channel ICF intracellular fluid ENS enteric nervous system IGF-I insulin-like growth factor I (somatomedin C) EPP equal pressure point I/G ratio insulin/glucagon ratio EPSP excitatory postsynaptic potential I ion ionic current ER endoplasmic reticulum IJP inhibitory junction potential ERV expiratory reserve volume IL interleukin ESR erythrocyte sedimentation rate IP 3 inositol 1,4,5-trisphosphate ESV end-systolic volume IPSP inhibitory postsynaptic potential F fractional concentration of gas; farad; Faraday IRDS infant respiratory distress syndrome constant IRV inspiratory reserve volume f frequency J flow (or flux) of a solute or water; joule FEF forced expiratory flow K heat loss by conduction FEV forced expiratory volume K f ultrafiltration coefficient FGF fibroblast growth factor K h hydraulic conductivity FL focal length L lung FM frequency modulation LDL low-density lipoprotein FRC functional residual capacity L-DOPA L-3,4-dihydroxyphenylalanine FSH follicle-stimulating hormone LH luteinizing hormone FVC forced vital capacity LHRH luteinizing hormone-releasing hormone g ionic conductance M metabolic rate G protein guanine nucleotide-binding protein MAP microtubule-associated protein GABA -aminobutyric acid MAP kinase mitogen-activated protein kinase GAP GnRH-associated peptide MCH mean cell (corpuscular) hemoglobin GC glomerular capillary MCHC mean cell (corpuscular) hemoglobin GDP guanosine diphosphate concentration GFR glomerular filtration rate MCR metabolic clearance rate GH growth hormone (somatotropin) M-CSF macrophage-colony stimulating factor GHRH growth hormone-releasing hormone MCV mean cell (corpuscular) volume GI gastrointestinal MIT monoiodotyrosine GIP gastric inhibitory peptide (glucose-dependent MLCK myosin light-chain kinase insulinotropic peptide) MLCP myosin light-chain phosphatase GLP glucagon-like peptide MMC migrating motor complex GLUT glucose transporter MSH melanocyte-stimulating hormone GnRH gonadotropin-releasing hormone (LHRH) MVC maximal voluntary contraction GPCR G-protein-coupled receptor NANC nonadrenergic noncholinergic GRE glucocorticoid response element NaPi sodium-coupled phosphate transporter GRP gastrin-releasing peptide NE norepinephrine GTO Golgi tendon organ NHE Na /H exchanger GTP guanosine triphosphate NK natural killer Hb hemoglobin NMDA N-methyl-D-aspartate convective heat transfer coefficient NO nitric oxide h c hCG human chorionic gonadotropin NOS nitric oxide synthase HDL high-density lipoprotein N R Reynolds number evaporative heat transfer coefficient OAT organic anion transporter h e HF heat flow OCT organic cation transporter HGF hepatocyte growth factor P pressure; partial pressure; permeability; hPL human placental lactogen (human chorionic permeability coefficient; plasma; plasma somatomammotropin) concentration HR heart rate P 50 PO 2 at which 50% of hemoglobin is saturated HRE hormone response element PAH p-aminohippurate HSL hormone-sensitive lipase Pc
pulmonary end-capillary 5-HT 5-hydroxytryptamine (serotonin) PCr phosphocreatine (creatine phosphate) 5-HTP 5-hydroxytryptophan PDE phosphodiesterase I inspiratory PEF peak expiratory flow

APPENDIX B Common Abbreviations in Physiology 739 PG prostaglandin SVR systemic vascular resistance (total peripheral PI phosphatidylinositol resistance) inorganic phosphate SW stroke work P i PIF peak inspiratory flow T tension; temperature; time phosphatidylinositol 4,5-bisphosphate triiodothyronine PIP 2 T 3 PKA protein kinase A T 4 thyroxine PKC protein kinase C Ttidal PKG cGMP-dependent protein kinase ttime pl pleural ta transairway PLC phospholipase C TBG thyroxine-binding globulin PNS peripheral nervous system TBW total body water POMC proopiomelanocortin TEA tetraethylammonium PRL prolactin TF tubule fluid PRU peripheral resistance unit TGF transforming growth factor PT prothrombin time TLC total lung capacity PTH parathyroid hormone (parathormone) tm transmural PTT partial thromboplastin time Tm tubular transport maximum PVC premature ventricular complex Tn-C calcium-binding troponin pw pulmonary wedge TNF tumor necrosis factor ˙ Q blood flow Tn-I troponin that inhibits actin-myosin R respiratory exchange ratio; resistance; interactions universal gas constant Tn-T tropomyosin-binding troponin R heat loss by radiation tp transpulmonary r radius; radiant environment TPA tissue plasminogen activator RAAS renin-angiotensin-aldosterone system TR thyroid hormone receptor RBF renal blood flow TRE thyroid hormone response element RBP retinol-binding protein TRH thyrotropin-releasing hormone RDA recommended daily allowance TSC thiazide-sensitive (Na -Cl ) cotransporter REM rapid eye movement TSH thyroid-stimulating hormone rh relative humidity T tubule transverse tubule RIA radioimmunoassay U urine concentration RISA radioiodinated serum albumin UCP uncoupling protein ROS reactive oxygen species UDP uridine diphosphate RPF renal plasma flow UP ultrafiltration pressure gradient RQ respiratory quotient v velocity; venous RV residual volume V volume; volt; vasopressin; vacuolar RVD regulatory volume decrease V ˙ gas volume per unit time (airflow); minute RVI regulatory volume increase ventilation; urine flow rate ˙ S saturation; siemens VA alveolar ventilation s shunt VC vital capacity S rate of heat storage in the body VEGF vascular endothelial growth factor SA sinoatrial VIP vasoactive intestinal peptide SF-1 steroidogenic factor-1 VLDL very low density lipoprotein ˙ SGLT Na -glucose cotransporter VO 2 oxygen uptake SH2 src homology domain W heat loss as mechanical work SHBG sex hormone-binding globulin w wettedness SIADH syndrome of inappropriate ADH z valence of an ion sk skin  osmotic coefficient SN single nephron  viscosity SPCA serum prothrombin conversion accelerator  length (space) constant; wavelength SRIF somatotropin release inhibiting factor  electrochemical potential (somatostatin)  osmotic pressure; 3.14 (pi) SRY sex-determining region, Y chromosome density SSRI selective serotonin reuptake inhibitor reflection coefficient StAR steroidogenic acute regulatory protein  time constant SV stroke volume