front 1 (...) are secreted into the circulation in small amounts and delivered to target tissues, where they produce physiologic responses. | back 1 hormones |
front 2 What are the nine classic endocrine glands? | back 2 ![]()
(The kidney also is considered to be an endocrine gland) |
front 3 Hormones are categorized in one of three classes: (...). | back 3 peptides, steroids, or amines |
front 4 Most hormones are classified as peptides; in the nucleus, the gene for the peptide hormone is transcribed into an (...). | back 4 mRNA |
front 5 The mRNA for the peptide hormone is transferred to the cytoplasm and translated on the ribosomes to the first protein product, a (...). | back 5 preprohormone |
front 6 The signal peptide is removed from the preprohormone in the endoplasmic reticulum, converting the it to a (...). | back 6 prohormone |
front 7 The prohormone is transferred to the Golgi apparatus, where it is packaged in (...). | back 7 secretory vesicles |
front 8 In the secretory vesicles, proteolytic enzymes cleave peptide sequences from the prohormone to produce the final (...). | back 8 hormone |
front 9 The final hormone is stored in (...) until the endocrine cell is stimulated. | back 9 ![]() secretory vesicles |
front 10 The steroid hormones are cortisol, aldosterone, estradiol and estriol, progesterone, testosterone, and 1,25-dihydroxycholecalciferol, which are derivatives of (...). | back 10 cholesterol |
front 11 The amine hormones are catecholamines and thyroid hormones, which are derivatives of the amino acid (...). | back 11 tyrosine |
front 12 Adjustments in secretory rates of hormones may be accomplished by (...) mechanisms or by (...) mechanisms. | back 12 neural; feedback |
front 13 (...) mechanisms of hormone control are illustrated by the secretion of catecholamines. | back 13 neural |
front 14 (...) mechanisms are the most common mechanism of hormone control. | back 14 feedback |
front 15 (...) feedback means that some feature of hormone action inhibits further secretion of the hormone. | back 15 ![]() negative |
front 16 (...) feedback means that the hormone feeds back all the way to the hypothalamic-pituitary axis. | back 16 long-loop |
front 17 (...) feedback means that the anterior pituitary hormone feeds back on the hypothalamus. | back 17 short-loop |
front 18 (...) feedback means that the hypothalamic hormone inhibits its own secretion. | back 18 ultrashort-loop |
front 19 (...) feedback is an uncommon mechanism of hormone control in which some feature of hormone action causes more secretion of the hormone. | back 19 ![]() positive |
front 20 The primary example of positive feedback is the effect of (...) on the secretion of gonadotropins by the anterior pituitary at the midpoint of the menstrual cycle. | back 20 estrogen |
front 21 A second example of hormonal positive feedback is (...), which is secreted by the posterior pituitary in response to dilation of the cervix. | back 21 oxytocin |
front 22 The responsiveness of a target tissue to a hormone is expressed in the (...) in which the magnitude of response is correlated with hormone concentration. | back 22 dose-response relationship |
front 23 (...) is defined as the hormone concentration that produces 50% of the maximal response. | back 23 sensitivity |
front 24 (...) means that the number or the affinity of the receptors for the hormone has decreased. | back 24 down-regulation |
front 25 (...) means that the number or the affinity of the receptors for the hormone has increased. | back 25 up-regulation |
front 26 The major mechanisms of hormone action on target cells are (1) the (...) mechanism, in which cAMP is the second messenger; (2) the (...) mechanism, in which IP3/Ca2+ is the second messenger; and (3) the (...) mechanism. | back 26 adenylyl cyclase; phospholipase C; steroid hormone |
front 27 Insulin and insulin-like growth factors (IGFs) act on their target cells through a (...) mechanism. | back 27 tyrosine kinase |
front 28 Several hormones activate (...), in which cyclic guanosine monophosphate is the second messenger. | back 28 guanylate cyclase |
front 29 G proteins can be either stimulatory or inhibitory and are called, accordingly, (...). | back 29 Gs (stimulatory) or Gi (inhibitory) |
front 30 When no hormone is bound to the receptor, the αs subunit of the Gs protein binds (...); In this configuration, the Gs protein is (...). | back 30 GDP; inactive |
front 31 When hormone binds to its receptor in the cell membrane, (...) is released from the αs subunit and is replaced by (...), and the (...) detaches from the Gs protein. | back 31 GDP; GTP; αs subunit |
front 32 The αs-GTP complex migrates within the cell membrane and binds to and activates (...). | back 32 adenylyl cyclase |
front 33 Activated adenylyl cyclase catalyzes the conversion of adenosine triphosphate (ATP) to (...), which serves as the second messenger. | back 33 cAMP |
front 34 cAMP, via a series of steps involving activation of (...), phosphorylates intracellular proteins. | back 34 protein kinase A |
front 35 Intracellular cAMP is degraded to an inactive metabolite, (...), by the enzyme (...), thereby turning off the action of the second messenger. | back 35 ![]() 5′ adenosine monophosphate (5′ AMP); phosphodiesterase |
front 36 With no hormone bound to the receptor, the αq subunit binds (...); In this configuration, the Gq protein is (...). | back 36 GDP; inactive |
front 37 When hormone binds to its receptor in the cell membrane, (...) is released from the αq subunit and is replaced by (...), and the (...) detaches from the Gq protein. | back 37 GDP; GTP; αq subunit |
front 38 The αq-GTP complex migrates within the cell membrane and binds to and activates (...). | back 38 phospholipase C |
front 39 Activated phospholipase C catalyzes the liberation of (...) and (...) from phosphatidylinositol 4,5-diphosphate (PIP2). | back 39 diacylglycerol; IP3 |
front 40 The IP3 causes the release of (...) from intracellular stores in the endoplasmic or sarcoplasmic reticulum. | back 40 Ca2+ |
front 41 Ca2+ and diacylglycerol activate (...), which phosphorylates proteins and produces the final physiologic actions. | back 41 ![]() protein kinase C |
front 42 Some hormones bind to cell surface receptors called (...) that have, or are associated with, enzymatic activity on the intracellular side. | back 42 catalytic receptors |
front 43 What are the four types of catalytic receptors? | back 43
|
front 44 Atrial natriuretic peptide (ANP) acts through a (...) mechanism. | back 44 receptor guanylyl cyclase |
front 45 Nitric oxide (NO) acts through a (...) mechanism. | back 45 cytosolic guanylyl cyclase |
front 46 (...) and (...) phosphorylate serine and threonine in the cascade of events leading to their biologic actions. | back 46 Ca2+-calmodulin-dependent protein kinase (CaMK); mitogen-activated protein kinases (MAPKs) |
front 47 (...) have intrinsic tyrosine kinase activity within the receptor molecule; (...) do not have intrinsic tyrosine kinase activity but associate with proteins that do. | back 47 ![]() receptor tyrosine kinases; tyrosine kinase–associated receptors |
front 48 The tyrosine kinase receptor for nerve growth factor (NGF) and epidermal growth factor receptors is a (...) which (...) after binding of ligand. | back 48 monomer; dimerizes |
front 49 The tyrosine kinase receptor for insulin and insulin-like growth factor (IGF) is a already a (...). | back 49 dimer |
front 50 The tyrosine kinase–associated receptor for growth hormone receptors is noncovalently “associated” with the (...) pathway. | back 50 JAK-STAT |
front 51 In contrast to peptide hormones, steroid hormones and thyroid hormones bind to (...) receptors and have a (...) onset of action. | back 51 cytosolic (or nuclear); slower (taking hours) |
front 52 The steroid hormone diffuses across the cell membrane, where it binds to a specific (...) that is located in either the cytosol or nucleus. | back 52 receptor protein |
front 53 The steroid hormone binds in the (...) of the steroid receptor protein located near the C terminus. | back 53 E domain |
front 54 The central (...) of the steroid receptor protein is highly conserved, has two zinc fingers, and is responsible for DNA binding. | back 54 ![]() C domain |
front 55 The steroid hormone-receptor complex dimerizes and binds (at its C domain) via the zinc fingers to specific DNA sequences, called (...). | back 55 steroid-responsive elements (SREs) |
front 56 After binding to the SRE, the hormone-receptor complex has now become a (...) that regulates the rate of transcription of that gene. | back 56 ![]() transcription factor |
front 57 The posterior lobe (or posterior pituitary) of the hypothalamus is also called the (...). | back 57 neurohypophysis |
front 58 The anterior lobe (or anterior pituitary) of the hypothalamus is also called the (...). | back 58 adenohypophysis |
front 59 The hypothalamus is connected to the pituitary gland by a thin stalk called the (...). | back 59 infundibulum |
front 60 The posterior lobe of the pituitary gland is derived from (...). | back 60 neural tissue |
front 61 What are the two hormones secreted by the posterior pituitary? | back 61
|
front 62 The hormones secreted by the posterior lobe are actually (...); in other words, they are peptides released from neurons. | back 62 neuropeptides |
front 63 Although both posterior pituitary hormones are synthesized in both nuclei, ADH is primarily associated with (...) and oxytocin is primarily associated with (...). | back 63 supraoptic nuclei; paraventricular nuclei |
front 64 Unlike the posterior lobe, which is neural tissue, the anterior lobe is primarily a collection of (...). | back 64 endocrine cells |
front 65 What are the six hormones secreted by the anterior pituitary? | back 65
|
front 66 The hypothalamus and anterior pituitary are linked directly by the (...), which provide most of the blood supply of the anterior lobe. | back 66 ![]() hypothalamic-hypophysial portal blood vessels |
front 67 What are the five major endocrine cell types of the anterior pituitary? | back 67
|
front 68 TSH, FSH, and LH are all (...) consisting of two subunits, α and β. | back 68 glycoproteins |
front 69 The (...) of TSH, FSH, and LH are identical and are synthesized from the same mRNA. | back 69 α subunits |
front 70 The (...) for TSH, FSH, and LH are different and therefore confer the biologic specificity. | back 70 β subunits |
front 71 The placental hormone (...) is structurally related to the TSH-FSH-LH family. | back 71 human chorionic gonadotropin (HCG) |
front 72 The ACTH family of hormones is derived from a single precursor, (...). | back 72 ![]() pro-opiomelanocortin (POMC) |
front 73 In (...), POMC and ACTH levels are increased by negative feedback, and because of their MSH activity, skin pigmentation is a symptom of this disorder. | back 73 Addison disease (primary adrenal insufficiency) |
front 74 (...) is secreted throughout life and is the single most important hormone for normal growth to adult stature. | back 74 growth hormone |
front 75 Growth hormone is synthesized in the somatotrophs of the anterior lobe of the pituitary and also is called (...). | back 75 somatotropin |
front 76 Human growth hormone is structurally similar to (...), containing 191 amino acids in a straight-chain polypeptide with 2 internal disulfide bridges. | back 76 prolactin |
front 77 Growth hormone is secreted in a (...) pattern, with bursts of secretion occurring approximately every 2 hours. | back 77 pulsatile |
front 78 At (...), there is an secretory burst of growth hormone, induced in females by estrogen and in males by testosterone. | back 78 puberty |
front 79 (...) and (...) are potent stimuli for growth hormone secretion. | back 79 ![]() hypoglycemia; starvation |
front 80 (...) acts directly on somatotrophs of the anterior pituitary to stimulate both synthesis and secretion of growth hormone. | back 80 GHRH |
front 81 (...) is also secreted by the hypothalamus and acts on the somatotrophs to inhibit growth hormone secretion. | back 81 somatostatin (SRIF) |
front 82 Growth hormone secretion is regulated by negative feedback: (1) GHRH is inhibited by (...); (2) growth hormone is inhibited by (...); (3) somatostatin is stimulated by (...). | back 82 ![]() GHRH (ultra-short loop); somatomedins; growth hormone and somatomedins |
front 83 The direct actions of growth hormone are mediated by (...) receptors in skeletal muscle, the liver, or adipose tissue. | back 83 tyrosine kinase–associated |
front 84 The indirect actions of growth hormone are mediated through the production of (...) in the liver, the most important of which is (...). | back 84 somatomedins (or IGFs); somatomedin C (or IGF-1) |
front 85 Somatomedins act on target tissues through IGF receptors that are similar to the insulin receptor, having (...) activity. | back 85 intrinsic tyrosine kinase |
front 86 What are the major actions of growth hormone? (3) | back 86
|
front 87 Growth hormone deficiency in children causes (...), including failure to grow, short stature, mild obesity, and delayed puberty. | back 87 dwarfism |
front 88 One variant of dwarfism is (...), in which growth hormone levels are elevated due to a defect in the growth hormone receptors. | back 88 Laron dwarfism |
front 89 Growth hormone excess causes (...) and is most often due to a growth hormone–secreting pituitary adenoma. | back 89 acromegaly |
front 90 Before puberty, excessive levels of growth hormone cause (...) because of intense hormonal stimulation at the epiphyseal plates. | back 90 gigantism |
front 91 Conditions with excess secretion of growth hormone are treated with (...), which inhibit growth hormone secretion by the anterior pituitary. | back 91 somatostatin analogues (e.g. octreotide) |
front 92 (...) is the major hormone responsible for milk production and also participates in the development of the breasts. | back 92 prolactin |
front 93 Chemically, prolactin is related to (...), having 198 amino acids in a single-chain polypeptide with 3 internal disulfide bridges. | back 93 growth hormone |
front 94 In persons who are not pregnant or lactating, prolactin secretion is tonically inhibited by (...) from the hypothalamus. | back 94 dopamine (prolactin-inhibiting factor) |
front 95 Prolactin inhibits its own secretion by increasing the synthesis and secretion of (...) from the hypothalamus. | back 95 ![]() dopamine |
front 96 (...) and (...) are the most important stimuli for prolactin secretion. | back 96 ![]() pregnancy; breast-feeding (suckling) |
front 97 What are the major actions of prolactin? (3) | back 97
|
front 98 Prolactin inhibits ovulation by inhibiting the synthesis and release of (...), which accounts for the decreased fertility during breast-feeding. | back 98 gonadotropin-releasing hormone (GnRH) |
front 99 Prolactin deficiency can be caused by total destruction of the (...) or selective destruction of (...). | back 99 destruction of the anterior pituitary; lactotrophs |
front 100 Prolactin excess can be caused by destruction of the (...) or by prolactin- secreting tumors called (...). | back 100 destruction of the hypothalamus; prolactinomas |
front 101 The major symptoms of excess prolactin secretion are (...) and (...). | back 101 galactorrhea; infertility |
front 102 Whether the result of hypothalamic failure or a prolactinoma, prolactin excess can be treated by administration of (...), a dopamine agonist. | back 102 bromocriptine |
front 103 ADH and oxytocin are homologous (...) (containing nine amino acids) synthesized in the supraoptic and paraventricular nuclei of the hypothalamus. | back 103 ![]() nonapeptides |
front 104 The ADH neurons have their cell bodies primarily in the (...) nuclei of the hypothalamus. | back 104 supraoptic nuclei |
front 105 The oxytocin neurons have their cell bodies primarily in (...) nuclei of the hypothalamus. | back 105 paraventricular |
front 106 The peptide precursor for ADH is (...), which comprises a signal peptide, ADH, neurophysin II, and a glycoprotein. | back 106 ![]() prepropressophysin |
front 107 The precursor for oxytocin is (...), which comprises a signal peptide, oxytocin, and neurophysin I. | back 107 ![]() prepro-oxyphysin |
front 108 (...) is the major hormone concerned with regulation of body fluid osmolarity. | back 108 ADH (or vasopressin) |
front 109 (...) is the most important physiologic stimulus for increasing ADH secretion. | back 109 ![]() increased plasma osmolarity |
front 110 (...) is a potent stimulus for ADH secretion which overrides plasma osmolarity. | back 110 ![]() hypovolemia |
front 111 What are the major actions of ADH? (2) | back 111
|
front 112 The receptor for ADH on the principal cells of the kidney is the (...) receptor, which is coupled to (...) via a G protein. | back 112 V2; adenylyl cyclase |
front 113 The second messenger for the V2 receptor is (...), which, via phosphorylation steps, directs the insertion of (...) in the luminal membranes. | back 113 cAMP; aquaporin 2 (AQP2) |
front 114 The receptor for ADH on vascular smooth muscle is the (...) receptor, which is coupled to (...) via a G protein. | back 114 V1; phospholipase C |
front 115 The second messenger for the V1 receptor is (...), which produces (...) of vascular smooth muscle. | back 115 contraction; IP3/Ca2+ |
front 116 (...) is caused by failure of the posterior pituitary to secrete ADH; the collecting ducts are impermeable to water, and the urine cannot be concentrated. | back 116 central diabetes insipidus |
front 117 Central diabetes insipidus is treated with an ADH analogue, (...). | back 117 desmopressin (dDAVP) |
front 118 In (...), the posterior pituitary is normal but the principal cells of the collecting duct are unresponsive to ADH due to a defect in the V2 receptor. | back 118 nephrogenic diabetes insipidus |
front 119 Nephrogenic diabetes insipidus is treated with (...). | back 119 thiazide diuretics |
front 120 In (...), excess ADH is secreted from an autonomous site, such as oat cell carcinoma of the lung. | back 120 syndrome of inappropriate ADH (SIADH) |
front 121 SIADH is treated with an ADH antagonist such as (...) or water restriction. | back 121 demeclocycline |
front 122 (...) produces milk “letdown” or milk ejection from the lactating breast. | back 122 oxytocin |
front 123 The major stimulus for oxytocin secretion is (...); however, (...) also cause milk letdown. | back 123 ![]() suckling; conditioned responses |
front 124 What are the major actions of oxytocin? (2) | back 124
|
front 125 Stimulation of powerful rhythmic contractions of uterine smooth muscle by oxytocin is the basis for its use in inducing (...) and in reducing (...). | back 125 labor; postpartum bleeding |
front 126 The two active thyroid hormones are (...) and (...). | back 126 ![]() triiodothyronine (T3); thyroxine (T4) |
front 127 Thyroid hormones are synthesized by the (...) cells of the thyroid gland. | back 127 ![]() follicular epithelial cells |
front 128 The material in the lumen of the follicles is (...), which is composed of newly synthesized thyroid hormones attached to (...). | back 128 colloid; thyroglobulin (TG) |
front 129 (...), a glycoprotein containing large quantities of tyrosine, is synthesized on the rough endoplasmic reticulum and the Golgi apparatus of the thyroid follicular cells. | back 129 thyroglobulin (TG) |
front 130 (...) is actively transported from blood into the thyroid follicular epithelial cells against both chemical and electrical gradients via (...). | back 130 I− (iodide); Na+-I− cotransport |
front 131 The anions (...) block Na+-I− cotransport into follicular cells and interfere with the synthesis of thyroid hormones. | back 131 thiocyanate and perchlorate |
front 132 Once I− is pumped into the follicular epithelial cell, it is oxidized to (...) by the enzyme (...). | back 132 I2 (iodide); thyroid peroxidase |
front 133 Thyroid peroxidase is inhibited by (...), which blocks the synthesis of thyroid hormones. | back 133 propylthiouracil (PTU) |
front 134 At the apical membrane, I2 combines with the (...) moieties of TG, catalyzed by thyroid peroxidase, to form (...) and (...). | back 134 tyrosine; monoiodotyrosine (MIT); diiodotyrosine (DIT) |
front 135 High levels of I− inhibit organification and synthesis of thyroid hormones, which is known as the (...). | back 135 Wolff-Chaikoff effect |
front 136 While still part of TG, coupling reactions occur between MIT and DIT; either two molecules of DIT combine to form (...) or DIT combines with MIT to form (...). | back 136 thyroxine (T4); triiodothyronine (T3) |
front 137 Iodinated TG is stored in the follicular lumen as (...) until the thyroid gland is stimulated to secrete its hormones (e.g., by TSH). | back 137 colloid |
front 138 When the thyroid gland is stimulated, iodinated TG is (...) into the follicular epithelial cells. | back 138 endocytosed |
front 139 (...) hydrolyze peptide bonds to release T4, T3, MIT, and DIT from TG. | back 139 lysosomal proteases |
front 140 MIT and DIT are deiodinated inside the follicular cell by the enzyme (...), then are incorporated into the synthesis of new TG to begin another cycle. | back 140 ![]() thyroid deiodinase |
front 141 Most T4 and T3 circulates bound to (...); because only free thyroid hormones are physiologically active, this provides a reservoir of hormones. | back 141 thyroxine-binding globulin (TBG) |
front 142 In (...), blood levels of TBG decrease because there is decreased protein synthesis, resulting in a transient (...) in the level of free thyroid hormones. | back 142 hepatic failure; increase |
front 143 During (...), high levels of estrogen inhibits hepatic breakdown of TBG, resulting in a transient (...) in the level of free thyroid hormones. | back 143 pregnancy; decrease |
front 144 Circulating levels of TBG can be indirectly assessed with the (...), which measures the binding of radioactive T3 to a synthetic resin. | back 144 T3 resin uptake test |
front 145 The major secretory product of the thyroid gland is (...), which is the less active form of thyroid hormone. | back 145 T4 |
front 146 In the target tissues, the enzyme (...) converts T4 to T3 by removing one atom of I2 from the outer ring of the molecule. | back 146 5′-iodinase |
front 147 The target tissues also convert a portion of the T4 to an inactive form, (...), by removing one atom of I2 from the inner ring of the molecule. | back 147 reverse T3 (rT3) |
front 148 (...) inhibits 5′-iodinase in tissues such as skeletal muscle, thus lowering O2 consumption and basal metabolic rate. | back 148 starvation |
front 149 (...) acts on the thyrotrophs of the anterior pituitary to stimulate synthesis and secretion of TSH. | back 149 TRH |
front 150 (...) regulates the growth of the thyroid gland (i.e. a trophic effect) and the secretion of thyroid hormones. | back 150 ![]() TSH |
front 151 TSH secretion is regulated by two reciprocal factors: (1) (...) stimulates the secretion of TSH; (2) (...) inhibits the secretion of TSH by down-regulating the TRH receptor. | back 151 ![]() TRH; thyroid hormone (i.e. free T3) |
front 152 The actions of TSH on the thyroid gland are initiated when TSH binds to a membrane receptor, which is coupled to (...) via a G protein. | back 152 adenylyl cyclase |
front 153 Activation of adenylyl cyclase generates (...), which serves as the second messenger for TSH. | back 153 cAMP |
front 154 The TSH receptor on the thyroid cells also is activated by (...), which are antibodies to the TSH receptor. | back 154 thyroid-stimulating immunoglobulins |
front 155 (...), a common form of hyperthyroidism, is caused by increased circulating levels of thyroid-stimulating immunoglobulins. | back 155 Graves disease |
front 156 The first step in the action of thyroid hormones in target tissues is (...). | back 156 conversion of T4 to T3 by 5′-iodinase |
front 157 Once T3 is produced inside the target cells, it binds to a (...). | back 157 nuclear receptor |
front 158 The T3-receptor complex then binds to a (...) on DNA, where it stimulates (...). | back 158 thyroid-regulatory element; DNA transcription |
front 159 A vast array of new proteins are synthesized under the direction of thyroid hormones, including (...). | back 159 Na+-K+ ATPase |
front 160 What are the major effects of thyroid hormones? (5) | back 160 ![]()
|
front 161 Thyroid hormones increase oxygen consumption in all tissues except (...) by inducing the synthesis and increasing the activity of (...). | back 161 brain, gonads, and spleen; Na+-K+ ATPase |
front 162 The cardiac effects of thyroid hormones are explained by the fact that they induce the synthesis of (...). | back 162 β1-adrenergic receptors |
front 163 Many of the effects of thyroid hormones on BMR, heat production, heart rate, and stroke volume are similar to those produced by catecholamines via (...) receptors. | back 163 β-adrenergic |
front 164 The most common form of hyperthyroidism is (...), an autoimmune disorder characterized by increased circulating levels of (...). | back 164 Graves disease; thyroid-stimulating immunoglobulins |
front 165 The diagnosis of hyperthyroidism is based on symptoms and measurement of increased levels of (...). | back 165 T3 and T4 |
front 166 If the cause of hyperthyroidism is a disorder of the thyroid gland, then TSH levels will be (...). | back 166 decreased |
front 167 If the cause of hyperthyroidism is a disorder of the hypothalamus or anterior pituitary, then TSH levels will be (...). | back 167 increased |
front 168 What are the symptoms of hyperthyroidism? (10) | back 168
|
front 169 Treatment of hyperthyroidism includes (...), which inhibits the synthesis of thyroid hormones, surgical removal of the gland, or radioactive ablation with (...) | back 169 propylthiouracil: 131I− |
front 170 The most common cause of hypothyroidism is (...) in which antibodies may either frankly destroy the gland or block thyroid hormone synthesis. | back 170 autoimmune destruction (thyroiditis) |
front 171 The diagnosis of hypothyroidism is based on symptoms and a finding of decreased levels of (...). | back 171 T3 and T4 |
front 172 If the cause of hypothyroidism is a disorder of the thyroid gland, then TSH levels will be (...). | back 172 increased |
front 173 If the cause of hypothyroidism is a disorder of the hypothalamus or anterior pituitary, then TSH levels will be (...). | back 173 decreased |
front 174 What are the symptoms of hypothyroidism? (10) | back 174
|
front 175 In some cases of hypothyroidism, (...) develops, in which there is edema due to accumulation of osmotically active mucopolysaccharides in interstitial fluid. | back 175 myxedema |
front 176 When the cause of hypothyroidism is a defect in the thyroid, a (...) develops from the unrelenting stimulation of the thyroid gland by TSH. | back 176 goiter |
front 177 If hypothyroidism occurs in the perinatal period and is untreated, it results in an irreversible form of growth and mental retardation called (...). | back 177 cretinism |
front 178 Treatment of hypothyroidism involves thyroid hormone replacement therapy, usually (...). | back 178 T4 (levothyroxine) |
front 179 Which of the following conditions are associated with goiter?
| back 179
|
front 180 The (...), which is in the inner zone of the adrenal gland that comprises 20% of the tissue, is of (...) origin and secretes (...). | back 180 adrenal medulla; neuroectodermal; catecholamines |
front 181 The (...), which is in the outer zone of the adrenal gland that comprises 80% of the tissue, is of (...) origin and secretes (...). | back 181 adrenal cortex; mesodermal; adrenocortical steroids |
front 182 The innermost zone of the adrenal cortex, called the (...), and the middle zone, called the (...), synthesize and secrete (...) and (...). | back 182 zona reticularis; zona fasciculata; glucocorticoids; adrenal androgens |
front 183 The outermost zone of the adrenal cortex, called the (...), secretes (...). | back 183 ![]() zona glomerulosa; mineralocorticoids |
front 184 All of the steroids of the adrenal cortex are chemical modifications of a basic steroid nucleus, which is illustrated in the structure of (...). | back 184 ![]() cholesterol |
front 185 The (...), represented by cortisol, have a ketone group at carbon 3 (C3) and hydroxyl groups at C11 and C21. | back 185 glucocorticoids |
front 186 The (...), represented by aldosterone, have a double-bond oxygen at C18. | back 186 mineralocorticoids |
front 187 The (...), represented in the adrenal cortex by dehydroepiandrosterone (DHEA) and androstenedione, have a double-bond oxygen at C17. | back 187 androgens |
front 188 The layers of the adrenal cortex are specialized to synthesize and secrete particular steroid hormones; the basis for this is the presence or absence of (...). | back 188 enzymes that catalyze modifications of the steroid nucleus |
front 189 The precursor for all adrenocortical steroids is (...). | back 189 cholesterol |
front 190 The enzymes catalyzing the conversion of cholesterol to active steroid hormones require (...), molecular oxygen, and NADPH. | back 190 cytochrome P-450 |
front 191 A flavoprotein enzyme called (...) and an iron-containing protein called (...) are intermediates in the transfer of hydrogen from NADPH to the cytochrome P-450 enzymes. | back 191 adrenodoxin reductase; adrenodoxin |
front 192 The first step in the synthesis of all adrenocortical steroid hormones, conversion of cholesterol to pregnenolone, is catalyzed by (...). | back 192 cholesterol desmolase |
front 193 Cholesterol desmolase, the rate-limiting enzyme in adrenocortical steroid hormone synthesis pathway, is stimulated by (...). | back 193 ![]() ACTH |
front 194 The major glucocorticoid produced in humans is (...), which is synthesized in the (...). | back 194 cortisol; zonae fasciculata and reticularis |
front 195 Cortisol is not the only steroid in the pathway with glucocorticoid activity; (...) is also a glucocorticoid. | back 195 ![]() corticosterone |
front 196 (...) inhibits 11β-hydroxylase, the last step in cortisol synthesis. | back 196 metyrapone |
front 197 (...) inhibits several steps in the pathway including cholesterol desmolase, the first step. | back 197 ketoconazole |
front 198 (...) are androgenic steroids produced in the (...). | back 198 DHEA and androstenedione; zonae fasciculata and reticularis |
front 199 Adrenal androgens have a ketone group at C17, thus they are also called (...). | back 199 17-ketosteroids |
front 200 The major mineralocorticoid in the body is (...), which is synthesized only in the (...). | back 200 aldosterone; zona glomerulosa |
front 201 The addition of the enzyme (...) in the zona glomerulosa allow the conversion of corticosterone to aldosterone. | back 201 aldosterone synthase |
front 202 Aldosterone is not the only steroid with mineralocorticoid activity; (...) and (...) also have mineralocorticoid activity. | back 202 ![]() 11-deoxycorticosterone (DOC); corticosterone |
front 203 The synthesis and secretion of steroid hormones by the adrenal cortex depend on the stimulation of cholesterol desmolase by (...). | back 203 ACTH |
front 204 The zonae fasciculata and reticularis, which secrete glucocorticoids and androgens, are under the exclusive control of the (...). | back 204 hypothalamic-pituitary axis |
front 205 The zona glomerulosa, which secretes mineralocorticoids, depends on ACTH for the first step in steroid biosynthesis, but otherwise it is controlled via the (...). | back 205 renin-angiotensin-aldosterone system |
front 206 An impressive feature of the regulation of cortisol secretion is its (...) nature and its (...) pattern. | back 206 ![]() pulsatile; diurnal (daily) |
front 207 The secretion of glucocorticoids by the zonae fasciculata/reticularis is regulated exclusively by the (...). | back 207 hypothalamic-pituitary axis |
front 208 (...) acts on the corticotrophs by an adenylyl cyclase/cAMP mechanism to cause secretion of ACTH into the bloodstream. | back 208 CRH |
front 209 (...) activates cholesterol desmolase in the adrenal cortex and up-regulates transcrption of its own receptor. | back 209 ACTH |
front 210 ACTH has a (...) secretory pattern that drives a parallel pattern of cortisol secretion. | back 210 ![]() pulsatile and diurnal |
front 211 Negative feedback is exerted by cortisol at three points in the hypothalamic-pituitary axis: (1) it directly inhibits (...); (2) it indirectly inhibits CRH secretion by effects on (...); (3) it inhibits the action of CRH on the (...). | back 211 ![]() CRH secretion; hippocampal neurons; anterior pituitary |
front 212 The (...) test is based on the negative feedback effects of cortisol on the CRH-ACTH axis. | back 212 dexamethasone suppression |
front 213 When a low dose of dexamethasone is given to a healthy person, it inhibits (...). | back 213 ACTH secretion |
front 214 The major use of the dexamethasone suppression test is in persons with (...). | back 214 hypercortisolism |
front 215 If the cause of hypercortisolism is (...), a low dose of dexamethasone does not suppress cortisol secretion but a high dose of dexamethasone does. | back 215 ACTH-secreting tumor |
front 216 If the cause of hypercortisolism is an (...), then neither low-dose nor high-dose dexamethasone suppresses cortisol secretion. | back 216 adrenal cortical tumor |
front 217 The major control of aldosterone secretion is via the (...). | back 217 renin–angiotensin II–aldosterone system |
front 218 The mediator of mineralcorticoid secretion is (...), which increases the synthesis and secretion of aldosterone by stimulating cholesterol desmolase and aldosterone synthase. | back 218 ![]() angiotensin II |
front 219 (...) is the enzyme that catalyzes the conversion of angiotensinogen to angiotensin I, which is inactive. | back 219 renin |
front 220 (...) catalyzes the conversion of angiotensin I to angiotensin II, which then acts on the zona glomerulosa to stimulate aldosterone synthesis. | back 220 angiotensin-converting enzyme (ACE) |
front 221 Increases in serum (...) concentration increase aldosterone secretion. | back 221 K+ |
front 222 What are the major actions of glucocorticoids? (7) | back 222
|
front 223 Glucocorticoids are essential for survival during (...) because they stimulate these gluconeogenic routes. | back 223 fasting |
front 224 Cortisol interferes with the body's inflammatory response by (1) inducing synthesis of (...), an inhibitor of phospholipase A2; (2) inhibiting production of (...), and proliferation of T lymphocytes; and (3) inhibiting release of (...) and (...) from mast cells and platelets. | back 224 lipocortin; interleukin-2 (IL-2); histamine; serotonin |
front 225 Aldosterone has three actions on the late distal tubule and collecting ducts:
| back 225 Na+; K+; H+ |
front 226 Renal cells contain the enzyme (...), which converts high-affinity cortisol to low affinity cortisone to prevent it from dominating mineralocorticoid receptors. | back 226 11β-hydroxysteroid dehydrogenase |
front 227 In (...), there is increased synthesis of adrenal androgens leading to masculinization in females and suppression of gonadal function in both males and females. | back 227 adrenogenital syndrome |
front 228 In the adrenogenital syndromes, due to the overproduction of adrenal androgens, there will be increased urinary levels of (...). | back 228 17-ketosteroids |
front 229 Cortisol promotes gluconeogenesis; therefore, excess levels produce (...) and deficits produce (...) upon fasting. | back 229 hyperglycemia; hypoglycemia |
front 230 Aldosterone causes increased K+ secretion by the renal principal cells; thus excess causes (...) and deficiency causes (...). | back 230 hypokalemia; hyperkalemia |
front 231 Because adrenal androgens have testosterone-like effects, in females, overproduction causes (...) and deficits result in (...). | back 231 masculinization; loss of pubic hair and libido |
front 232 (...) is commonly caused by autoimmune destruction of all zones of the adrenal cortex, resulting in decreased synthesis of all adrenocortical hormones. | back 232 Addison disease (primary adrenocortical insufficiency) |
front 233 Addison disease also is characterized by (...), particularly of the elbows, knees, nail beds, nipples, and areolae and on recent scars. | back 233 hyperpigmentation |
front 234 Hyperpigmentation in Addison disease is a result of increased levels of (...). | back 234 ACTH (contains the α-MSH fragment) |
front 235 Conditions of (...) occur when there is insufficient CRH or insufficient ACTH. | back 235 secondary adrenocortical insufficiency |
front 236 (...) is the result of chronic excess of glucocorticoids due to overproduction by the adrenal cortex or exogenous administration. | back 236 Cushing syndrome |
front 237 (...) is characterized by excess glucocorticoids, in which the cause is hypersecretion of ACTH from a pituitary adenoma. | back 237 Cushing disease |
front 238 What are the symptoms of Cushing syndrome? (8) | back 238
|
front 239 The (...), in which a synthetic glucocorticoid is administered, can distinguish between Cushing syndrome and Cushing disease. | back 239 dexamethasone suppression test |
front 240 In (...), because the tumor functions autonomously, cortisol secretion is not suppressed by either low- or high-dose dexamethasone. | back 240 Cushing syndrome |
front 241 In (...), ACTH and cortisol secretion are suppressed by high-dose dexamethasone but not by low-dose dexamethasone. | back 241 Cushing disease |
front 242 Treatment of Cushing syndrome includes administration of drugs such as (...), which block steroid hormone biosynthesis. | back 242 ketoconazole or metyrapone |
front 243 Because of its different etiology, treatment of Cushing disease involves (...). | back 243 surgical removal of the ACTH-secreting tumor |
front 244 (...) is caused by an aldosterone-secreting tumor. | back 244 Conn syndrome (primary hyperaldosteronism) |
front 245 Treatment of Conn syndrome consists of administration of an aldosterone antagonist such as (...), followed by surgical removal of the tumor. | back 245 spironolactone |
front 246 The most common enzymatic defect in the steroid hormone biosynthetic pathways is deficiency of (...), which belongs to a group of disorders called (...). | back 246 21β-hydroxylase; adrenogenital syndrome |
front 247 Without 21β-hydroxylase, the adrenal cortex is unable to convert progesterone to (...) or 17-hydroxyprogesterone to (...). | back 247 ![]() DOC; 11-deoxycortisol (the adrenal cortex does not synthesize mineralocorticoids or glucocorticoids) |
front 248 In 21β-hydroxylase deficiency, steroid intermediates will accumulate above the enzyme block and be shunted toward production of (...). | back 248 adrenal androgens (causes virilization in females) |
front 249 In 21β-hydroxylase deficiency, elevated ACTH (via negative feedback) has a trophic effect on the adrenal cortex; thus the other name for this disorder is (...). | back 249 congenital adrenal hyperplasia |
front 250 A less common congenital abnormality of the steroid hormone biosynthetic pathway is deficiency of (...). | back 250 17α-hydroxylase |
front 251 Without 17α-hydroxylase, pregnenolone cannot be converted to (...) and progesterone cannot be converted to (...). | back 251 ![]() 17-hydroxypregnenolone; 17-hydroxyprogesterone (neither glucocorticoids nor adrenal androgens will be produced) |
front 252 In this 17α-hydroxylase deficiency, steroid intermediates accumulate to the left of the enzyme block and will be shunted toward production of (...). | back 252 mineralocorticoids (causes hypertension, hypokalemia, and metabolic alkalosis) |
front 253 The endocrine cells of the pancreas are arranged in clusters called the (...), which compose 1% to 2% of the pancreatic mass. | back 253 ![]() islets of Langerhans |
front 254 The β cells compose 65% of the islet and secrete (...). | back 254 insulin |
front 255 The α cells compose 20% of the islet and secrete (...). | back 255 glucagon |
front 256 The delta (δ) cells compose 10% of the islet and secrete (...). | back 256 somatostatin |
front 257 The remaining cells of the pancreatic islets secrete (...). | back 257 pancreatic polypeptide |
front 258 Insulin is synthesized and secreted by the (...). | back 258 β cells |
front 259 Insulin is a peptide hormone consisting of two straight chains designated as the (...) and (...). | back 259 A chain; B chain |
front 260 The synthesis of insulin is directed by a gene on (...), a member of a superfamily of genes that encode related growth factors. | back 260 chromosome 11 |
front 261 The mRNA directs ribosomal synthesis of (...), which contains four peptides: a signal peptide, the A and B chains of insulin, and a connecting peptide (C peptide). | back 261 preproinsulin |
front 262 The signal peptide is cleaved from preproinsulin early in the biosynthetic process, yielding (...) | back 262 ![]() proinsulin |
front 263 Proinsulin is packaged in secretory granules on the Golgi apparatus, during which, proteases cleave the connecting peptide, yielding (...). | back 263 insulin |
front 264 The secretion of (...) is the basis of a test for β cell function in persons with type I diabetes mellitus who are receiving injections of exogenous insulin. | back 264 C peptide (It is packaged with insulin and released in equimolar quantities) |
front 265 The most important factor influencing the secretion of insulin by β cells is (...) | back 265 ![]() glucose |
front 266 The β cell membrane contains (...), a specific transporter for glucose that moves glucose from the blood into the cell by facilitated diffusion | back 266 GLUT2 |
front 267 Once inside the cell, glucose is phosphorylated to glucose-6-phosphate by (...), and glucose-6-phosphate is subsequently oxidized. | back 267 glucokinase |
front 268 Oxidation of glucose-6-phosphate generates (...), which appears to be the key factor that regulates insulin secretion. | back 268 ATP |
front 269 When ATP levels inside the β cell increase, the ATP-sensitive (...) channels close, which depolarizes the β cell membrane. | back 269 K+ |
front 270 The depolarization of the β cell caused by closure of the K+ channels opens voltage-sensitive (...) channels. | back 270 Ca2+ |
front 271 Increases in intracellular Ca2+ concentration within the β cell causes exocytosis of the (...)-containing secretory granules | back 271 ![]() insulin |
front 272 Oral glucose is a more powerful stimulant for insulin secretion than intravenous glucose because it stimulates the secretion of (...). | back 272 glucose-dependent insulinotropic peptide (GIP) |
front 273 (...) activates a Gq protein coupled to phospholipase C, which leads to a rise in intracellular Ca2+, causing exocytosis of insulin. | back 273 glucagon |
front 274 (...) inhibits the insulin-releasing mechanism that glucagon stimulates. | back 274 somatostatin |
front 275 (...) treat type II diabetes mellitus by stimulating insulin release from β cells by closing the ATP-dependent K+ channels. | back 275 sulfonylureas (e.g. tolbutamide, glyburide) |
front 276 The insulin receptor is a tetramer composed of two (...) and two (...), joined by disulfide bonds. | back 276 ![]() α subunits; β subunits |
front 277 The (...) of the insulin receptor have intrinsic tyrosine kinase activity. | back 277 β subunits |
front 278 Insulin binds to the (...) of the tetrameric insulin receptor, producing a conformational change in the receptor. | back 278 α subunits |
front 279 The conformational change in the α subunits of the insulin receptor activates tyrosine kinase in the β subunits, which (...) presence of ATP. | back 279 autophosphorylate |
front 280 Activated (...) on the β subunits phosphorylates several other proteins or enzymes that are involved in the physiologic actions of insulin. | back 280 tyrosine kinase |
front 281 Insulin (...) its own receptor by decreasing the rate of synthesis and increasing the rate of degradation of the receptor. | back 281 down-regulates |
front 282 What are the major actions of insulin? (4) | back 282 ![]()
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front 283 The hypoglycemic action of insulin is the result of (1) it increasing glucose transport into target cells by increasing (...) (2) it promoting (...) in the liver and in muscle and inhibiting (...); (3) it inhibiting gluconeogenesis by increasing the production of (...). | back 283 ![]() GLUT4; glycogenesis; glycogenolysis; fructose 2,6-bisphosphate |
front 284 Insulin also appears to have a direct effect on the hypothalamic (...) center independent of the changes it produces in blood glucose concentration. | back 284 satiety |
front 285 (...) is caused by destruction of β cells, often as a result of an autoimmune process. | back 285 type I (insulin-dependent) diabetes mellitus |
front 286 The increased levels of ketoacids in type I diabetes mellitus cause a form of metabolic acidosis called (...). | back 286 diabetic ketoacidosis (DKA) |
front 287 In diabetes mellitus, the nonreabsorbed glucose in the renal tubules acts as an osmotic solute in urine, producing (...). | back 287 osmotic diuresis |
front 288 (...) is often associated with obesity and is caused by down-regulation of insulin receptors in target tissues and insulin resistance. | back 288 type II (non–insulin-dependent) diabetes mellitus |
front 289 (...) can be used to treat type II diabetes mellitus by stimulating pancreatic insulin secretion, while (...) up-regulate insulin receptors on target tissues. | back 289 sulfonylureas (e.g. tolbutamide or glyburide); biguanides (e.g. metformin) |
front 290 Glucagon is synthesized and secreted by the (...) of the islets of Langerhans. | back 290 α cells |
front 291 The major factor stimulating the secretion of glucagon is (...). | back 291 decreased blood glucose concentration |
front 292 Glucagon secretion also is stimulated by the ingestion of protein, specifically by the amino acids (...) and (...). | back 292 arginine; alanine |
front 293 Another factor stimulating glucagon secretion is (...), which is secreted from the gastrointestinal tract when protein or fat is ingested. | back 293 ![]() cholecystokinin (CCK) |
front 294 The glucagon receptor is coupled to (...) via a G protein and second messenger is (...). | back 294 adenylyl cyclase; cAMP |
front 295 What are the major actions of glucagon? (2) | back 295 ![]()
|
front 296 Glucagon increases the blood glucose concentration by (1) stimulating (...) and inhibiting (...); and (2) by increasing gluconeogenesis by decreasing the production of (...). | back 296 ![]() glycogenolysis; glycogenesis; fructose 2,6-bisphosphate |
front 297 Pancreatic somatostatin is secreted by the (...) of the islets of Langerhans. | back 297 δ cells |
front 298 Pancreatic somatostatin inhibits secretion of (...) via paracrine actions. | back 298 insulin and glucagon |
front 299 The total Ca2+ concentration in blood is normally 10 mg/dL; (...) amounts to 50% of total Ca2+ and it is the only form that is biologically active. | back 299 ![]() free, ionized Ca2+ |
front 300 (...) is a decrease in the plasma Ca2+ concentration, which produces symptoms of hyperreflexia, spontaneous twitching, muscle cramps, and tingling and numbness. | back 300 hypocalcemia |
front 301 Specific indicators of hypocalcemia include the (...), or twitching of the facial muscles elicited by tapping on the facial nerve, and the (...), which is carpopedal spasm upon inflation of a blood pressure cuff. | back 301 Chvostek sign; Trousseau sign |
front 302 (...) is an increase in the plasma Ca2+ concentration, which produces symptoms of constipation, polyuria, polydipsia, hyporeflexia, lethargy, coma, and death. | back 302 hypercalcemia |
front 303 Changes in plasma (...) concentration alter the total Ca2+ concentration in the same direction. | back 303 protein |
front 304 Changes in plasma (...) concentration alter the ionized Ca2+ concentration by changing the fraction of complexed Ca2+. | back 304 anion |
front 305 (...) abnormalities alter the ionized Ca2+ concentration by changing the fraction of Ca2+ bound to plasma albumin. | back 305 acid-base |
front 306 In (...), there is more H+ in blood to bind to albumin, leaving fewer sites for Ca2+ to bind, thus the free ionized Ca2+ concentration (...). | back 306 ![]() acidemia; increases |
front 307 In (...), there is less H+ in blood to bind to albumin, leaving more sites for Ca2+ to bind, thus the free ionized Ca2+ concentration (...). | back 307 ![]() alkalemia; decreases |
front 308 What three organ systems are involved in Ca2+ homeostasis? | back 308 ![]() bone, kidney, and intestine |
front 309 The (...) of the parathyroid glands synthesize and secrete PTH. | back 309 chief cells |
front 310 PTH secretion is regulated by plasma (...) concentration; when it decreases to less than (...), PTH secretion is stimulated. | back 310 ![]() Ca2+; 10 mg/dL |
front 311 The parathyroid cell membrane contains (...) that are linked, via a G protein to phospholipase C. | back 311 Ca2+ sensing receptors |
front 312 Chronic (...) causes (...), which is characterized by increased synthesis and storage of PTH and hyperplasia of the parathyroid glands. | back 312 hypocalcemia; secondary hyperparathyroidism |
front 313 Chronic (...) causes decreased synthesis and storage of PTH, increased breakdown of stored PTH, and release of inactive PTH fragments into the circulation. | back 313 hypercalcemia |
front 314 (...) has parallel, although less important, effects on PTH secretion as Ca2+. | back 314 Mg2+ |
front 315 The receptor for PTH is coupled, via a G protein, to (...). | back 315 ![]() adenylyl cyclase |
front 316 In bone, PTH receptors are located only on (...). | back 316 osteoblasts |
front 317 Initially and transiently, PTH causes (...) by a direct action on osteoblasts. | back 317 increased bone formation |
front 318 In a second, long-lasting, indirect action on osteoclasts, PTH causes (...), mediated by (...) released from osteoblasts. | back 318 increased bone resorption; cytokines |
front 319 PTH inhibits (...) reabsorption in the proximal convoluted tubule. | back 319 phosphate (causes phosphaturia) |
front 320 The cAMP generated in cells of the proximal tubule is excreted in urine and is called (...). | back 320 nephrogenous or urinary cAMP |
front 321 The phosphaturic action of PTH is critical because otherwise the phosphate resorbed from bone would (...). | back 321 complex Ca2+ in ECF |
front 322 PTH stimulates (...) reabsorption in the proximal convoluted tubule. | back 322 Ca2+ |
front 323 PTH does not have direct actions on the small intestine, although indirectly it stimulates intestinal Ca2+ absorption via (...). | back 323 ![]() activation of vitamin D |
front 324 Primary hyperparathyroidism is most commonly caused by (...). | back 324 parathyroid adenomas (tumors) |
front 325 In primary hyperparathyroidism, (...) results from increased bone resorption, increased renal Ca2+ reabsorption, and increased intestinal Ca2+ absorption. | back 325 hypercalcemia |
front 326 In primary hyperparathyroidism, (...) results from decreased renal phosphate reabsorption and phosphaturia. | back 326 hypophosphatemia |
front 327 Persons with primary hyperparathyroidism are said to have "(...)." | back 327 “stones, bones, and groans” (stones from hypercalciuria, bones from increased bone resorption, and groans from constipation) |
front 328 In secondary hyperparathyroidism, the parathyroid glands are stimulated to secrete excessive PTH secondary to (...), which can be caused by (...). | back 328 hypocalcemia; vitamin D deficiency or chronic renal failure |
front 329 (...) is a relatively common, inadvertent consequence of thyroid surgery or parathyroid surgery. | back 329 hypoparathyroidism |
front 330 In hypoparathyroidism, (...) results from decreased bone resorption, decreased renal Ca2+ reabsorption, and decreased intestinal Ca2+ absorption. | back 330 hypocalcemia |
front 331 In hypoparathyroidism, (...) results from increased phosphate reabsorption. | back 331 hyperphosphatemia |
front 332 Patients with (...) have hypocalcemia and hyperphosphatemia; however, circulating levels of PTH are increased rather than decreased. | back 332 pseudohypoparathyroidism |
front 333 Pseudohypoparathyroidism is an inherited autosomal dominant disorder in which the (...) for PTH in kidney and bone is defective. | back 333 Gs protein |
front 334 Some malignant tumors secrete (...), which is structurally homologous with the PTH secreted by the parathyroid glands, with all the same physiologic actions. | back 334 PTH-related peptide (PTH-rp) |
front 335 Humoral hypercalcemia of malignancy is treated with (...), which inhibits renal Ca2+ reabsorption, and inhibitors of bone resorption such as (...). | back 335 furosemide; etidronate |
front 336 (...) is an autosomal dominant disorder characterized by decreased urinary Ca2+ excretion and increased serum Ca2+ concentration. | back 336 familial hypocalciuric hypercalcemia (FHH) |
front 337 FHH is caused by inactivating mutations of (...) in the parathyroid glands and the thick, ascending limb of the kidney. | back 337 Ca2+ sensing receptors |
front 338 Calcitonin is synthesized and secreted by the (...) of the thyroid gland. | back 338 parafollicular or C cells |
front 339 The major stimulus for calcitonin secretion is (...). | back 339 increased plasma Ca2+ concentration |
front 340 The major action of calcitonin is to (...), which decreases the plasma Ca2+ concentration. | back 340 inhibit bone resorption |
front 341 (...) in conjunction with PTH, is the second major regulatory hormone for Ca2+ and phosphate metabolism. | back 341 vitamin D |
front 342 Vitamin D in the form of (...) is provided in the diet and is produced in the skin from cholesterol. | back 342 cholecalciferol |
front 343 Cholecalciferol is physiologically inactive; it is hydroxylated in the liver to form (...), which also is inactive. | back 343 25-hydroxycholecalciferol |
front 344 In the kidney, 25-hydroxycholecalciferol (1) can be hydroxylated at C1 to produce (...), the active form, or (2) can be hydroxylated at C24 to produce (...), which is inactive. | back 344 ![]() 1,25-dihydroxycholecalciferol; 24,25-dihydroxycholecalciferol |
front 345 C1 hydroxylation of 25-hydroxycholecalciferol in the kidney is catalyzed by the enzyme (...). | back 345 1α-hydroxylase |
front 346 1α-hydroxylase activity is stimulated by(1) decreased plasma (...) concentration, (2) increased circulating levels of (...), and (3) decreased plasma (...) concentration. | back 346 Ca2+; PTH; phosphate |
front 347 The overall role of 1,25-dihydroxycholecalciferol is to increase the plasma concentration of (...) to promote (...). | back 347 Ca2+ and phosphate; mineralization of new bone |
front 348 In the intestine, 1,25-dihydroxycholecalciferol induces the synthesis of a vitamin D–dependent Ca2+-binding protein called (...). | back 348 ![]() calbindin D-28K |
front 349 The actions of 1,25-dihydroxycholecalciferol on the kidney are parallel to its actions on the intestine—it stimulates (...). | back 349 Ca2+ and phosphate reabsorption |
front 350 In bone, 1,25-dihydroxycholecalciferol acts synergistically with PTH to stimulate (...). | back 350 bone resorption (“old” bone is resorbed to provide Ca2+ and phosphate so that “new” bone can be mineralized) |
front 351 In children, vitamin D deficiency causes (...), a condition in which insufficient amounts of Ca2+ and phosphate are available to mineralize the growing bones. | back 351 rickets |
front 352 In adults, vitamin D deficiency results in (...), in which new bone fails to mineralize, resulting in bending and softening of the weight-bearing bones. | back 352 osteomalacia |
front 353 (...) occurs when the kidney is unable to produce the active metabolite, 1,25-dihydroxycholecalciferol. | back 353 vitamin D resistance |
front 354 Vitamin D resistance can be caused by the congenital absence of 1α-hydroxylase or, more commonly, by (...). | back 354 chronic renal failure |
front 355 ![]() | back 355 no data |
front 356 ![]() | back 356 no data |
front 357 ![]() | back 357 no data |
front 358 ![]() | back 358 no data |
front 359 ![]() | back 359 no data |