Physiology: Chapter 9: Endocrine Physiology Flashcards

(...) are secreted into the circulation in small amounts and delivered to target tissues, where they produce physiologic responses.

What are the nine classic endocrine glands?

Hormones are categorized in one of three classes: (...).

Most hormones are classified as peptides; in the nucleus, the gene for the peptide hormone is transcribed into an (...).

The mRNA for the peptide hormone is transferred to the cytoplasm and translated on the ribosomes to the first protein product, a (...).

The signal peptide is removed from the preprohormone in the endoplasmic reticulum, converting the it to a (...).

The prohormone is transferred to the Golgi apparatus, where it is packaged in (...).

In the secretory vesicles, proteolytic enzymes cleave peptide sequences from the prohormone to produce the final (...).

The final hormone is stored in (...) until the endocrine cell is stimulated.

The steroid hormones are cortisol, aldosterone, estradiol and estriol, progesterone, testosterone, and 1,25-dihydroxycholecalciferol, which are derivatives of (...).

The amine hormones are catecholamines and thyroid hormones, which are derivatives of the amino acid (...).

Adjustments in secretory rates of hormones may be accomplished by (...) mechanisms or by (...) mechanisms.

(...) mechanisms of hormone control are illustrated by the secretion of catecholamines.

(...) mechanisms are the most common mechanism of hormone control.

(...) feedback means that some feature of hormone action inhibits further secretion of the hormone.

(...) feedback means that the hormone feeds back all the way to the hypothalamic-pituitary axis.

(...) feedback means that the anterior pituitary hormone feeds back on the hypothalamus.

(...) feedback means that the hypothalamic hormone inhibits its own secretion.

(...) feedback is an uncommon mechanism of hormone control in which some feature of hormone action causes more secretion of the hormone.

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.

A second example of hormonal positive feedback is (...), which is secreted by the posterior pituitary in response to dilation of the cervix.

The responsiveness of a target tissue to a hormone is expressed in the (...) in which the magnitude of response is correlated with hormone concentration.

(...) is defined as the hormone concentration that produces 50% of the maximal response.

(...) means that the number or the affinity of the receptors for the hormone has decreased.

(...) means that the number or the affinity of the receptors for the hormone has increased.

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.

Insulin and insulin-like growth factors (IGFs) act on their target cells through a (...) mechanism.

Several hormones activate (...), in which cyclic guanosine monophosphate is the second messenger.

G proteins can be either stimulatory or inhibitory and are called, accordingly, (...).

When no hormone is bound to the receptor, the α_s subunit of the G_s protein binds (...); In this configuration, the G_s protein is (...).

When hormone binds to its receptor in the cell membrane, (...) is released from the α_s subunit and is replaced by (...), and the (...) detaches from the G_s protein.

The α_s-GTP complex migrates within the cell membrane and binds to and activates (...).

Activated adenylyl cyclase catalyzes the conversion of adenosine triphosphate (ATP) to (...), which serves as the second messenger.

cAMP, via a series of steps involving activation of (...), phosphorylates intracellular proteins.

Intracellular cAMP is degraded to an inactive metabolite, (...), by the enzyme (...), thereby turning off the action of the second messenger.

With no hormone bound to the receptor, the α_q subunit binds (...); In this configuration, the G_q protein is (...).

When hormone binds to its receptor in the cell membrane, (...) is released from the α_q subunit and is replaced by (...), and the (...) detaches from the G_q protein.

The α_q-GTP complex migrates within the cell membrane and binds to and activates (...).

Activated phospholipase C catalyzes the liberation of (...) and (...) from phosphatidylinositol 4,5-diphosphate (PIP₂).

The IP₃ causes the release of (...) from intracellular stores in the endoplasmic or sarcoplasmic reticulum.

Ca²⁺ and diacylglycerol activate (...), which phosphorylates proteins and produces the final physiologic actions.

Some hormones bind to cell surface receptors called (...) that have, or are associated with, enzymatic activity on the intracellular side.

What are the four types of catalytic receptors?

Atrial natriuretic peptide (ANP) acts through a (...) mechanism.

Nitric oxide (NO) acts through a (...) mechanism.

(...) and (...) phosphorylate serine and threonine in the cascade of events leading to their biologic actions.

(...) have intrinsic tyrosine kinase activity within the receptor molecule; (...) do not have intrinsic tyrosine kinase activity but associate with proteins that do.

The tyrosine kinase receptor for nerve growth factor (NGF) and epidermal growth factor receptors is a (...) which (...) after binding of ligand.

The tyrosine kinase receptor for insulin and insulin-like growth factor (IGF) is a already a (...).

The tyrosine kinase–associated receptor for growth hormone receptors is noncovalently “associated” with the (...) pathway.

In contrast to peptide hormones, steroid hormones and thyroid hormones bind to (...) receptors and have a (...) onset of action.

The steroid hormone diffuses across the cell membrane, where it binds to a specific (...) that is located in either the cytosol or nucleus.

The steroid hormone binds in the (...) of the steroid receptor protein located near the C terminus.

The central (...) of the steroid receptor protein is highly conserved, has two zinc fingers, and is responsible for DNA binding.

The steroid hormone-receptor complex dimerizes and binds (at its C domain) via the zinc fingers to specific DNA sequences, called (...).

After binding to the SRE, the hormone-receptor complex has now become a (...) that regulates the rate of transcription of that gene.

The posterior lobe (or posterior pituitary) of the hypothalamus is also called the (...).

The anterior lobe (or anterior pituitary) of the hypothalamus is also called the (...).

The hypothalamus is connected to the pituitary gland by a thin stalk called the (...).

The posterior lobe of the pituitary gland is derived from (...).

What are the two hormones secreted by the posterior pituitary?

The hormones secreted by the posterior lobe are actually (...); in other words, they are peptides released from neurons.

Although both posterior pituitary hormones are synthesized in both nuclei, ADH is primarily associated with (...) and oxytocin is primarily associated with (...).

Unlike the posterior lobe, which is neural tissue, the anterior lobe is primarily a collection of (...).

What are the six hormones secreted by the anterior pituitary?

The hypothalamus and anterior pituitary are linked directly by the (...), which provide most of the blood supply of the anterior lobe.

What are the five major endocrine cell types of the anterior pituitary?

TSH, FSH, and LH are all (...) consisting of two subunits, α and β.

The (...) of TSH, FSH, and LH are identical and are synthesized from the same mRNA.

The (...) for TSH, FSH, and LH are different and therefore confer the biologic specificity.

The placental hormone (...) is structurally related to the TSH-FSH-LH family.

The ACTH family of hormones is derived from a single precursor, (...).

In (...), POMC and ACTH levels are increased by negative feedback, and because of their MSH activity, skin pigmentation is a symptom of this disorder.

(...) is secreted throughout life and is the single most important hormone for normal growth to adult stature.

Growth hormone is synthesized in the somatotrophs of the anterior lobe of the pituitary and also is called (...).

Human growth hormone is structurally similar to (...), containing 191 amino acids in a straight-chain polypeptide with 2 internal disulfide bridges.

Growth hormone is secreted in a (...) pattern, with bursts of secretion occurring approximately every 2 hours.

At (...), there is an secretory burst of growth hormone, induced in females by estrogen and in males by testosterone.

(...) and (...) are potent stimuli for growth hormone secretion.

(...) acts directly on somatotrophs of the anterior pituitary to stimulate both synthesis and secretion of growth hormone.

(...) is also secreted by the hypothalamus and acts on the somatotrophs to inhibit growth hormone secretion.

Growth hormone secretion is regulated by negative feedback: (1) GHRH is inhibited by (...); (2) growth hormone is inhibited by (...); (3) somatostatin is stimulated by (...).

The direct actions of growth hormone are mediated by (...) receptors in skeletal muscle, the liver, or adipose tissue.

The indirect actions of growth hormone are mediated through the production of (...) in the liver, the most important of which is (...).

Somatomedins act on target tissues through IGF receptors that are similar to the insulin receptor, having (...) activity.

What are the major actions of growth hormone? (3)

Growth hormone deficiency in children causes (...), including failure to grow, short stature, mild obesity, and delayed puberty.

One variant of dwarfism is (...), in which growth hormone levels are elevated due to a defect in the growth hormone receptors.

Growth hormone excess causes (...) and is most often due to a growth hormone–secreting pituitary adenoma.

Before puberty, excessive levels of growth hormone cause (...) because of intense hormonal stimulation at the epiphyseal plates.

Conditions with excess secretion of growth hormone are treated with (...), which inhibit growth hormone secretion by the anterior pituitary.

(...) is the major hormone responsible for milk production and also participates in the development of the breasts.

Chemically, prolactin is related to (...), having 198 amino acids in a single-chain polypeptide with 3 internal disulfide bridges.

In persons who are not pregnant or lactating, prolactin secretion is tonically inhibited by (...) from the hypothalamus.

Prolactin inhibits its own secretion by increasing the synthesis and secretion of (...) from the hypothalamus.

(...) and (...) are the most important stimuli for prolactin secretion.

What are the major actions of prolactin? (3)

Prolactin inhibits ovulation by inhibiting the synthesis and release of (...), which accounts for the decreased fertility during breast-feeding.

Prolactin deficiency can be caused by total destruction of the (...) or selective destruction of (...).

Prolactin excess can be caused by destruction of the (...) or by prolactin- secreting tumors called (...).

The major symptoms of excess prolactin secretion are (...) and (...).

Whether the result of hypothalamic failure or a prolactinoma, prolactin excess can be treated by administration of (...), a dopamine agonist.

ADH and oxytocin are homologous (...) (containing nine amino acids) synthesized in the supraoptic and paraventricular nuclei of the hypothalamus.

The ADH neurons have their cell bodies primarily in the (...) nuclei of the hypothalamus.

The oxytocin neurons have their cell bodies primarily in (...) nuclei of the hypothalamus.

The peptide precursor for ADH is (...), which comprises a signal peptide, ADH, neurophysin II, and a glycoprotein.

The precursor for oxytocin is (...), which comprises a signal peptide, oxytocin, and neurophysin I.

(...) is the major hormone concerned with regulation of body fluid osmolarity.

(...) is the most important physiologic stimulus for increasing ADH secretion.

(...) is a potent stimulus for ADH secretion which overrides plasma osmolarity.

What are the major actions of ADH? (2)

The receptor for ADH on the principal cells of the kidney is the (...) receptor, which is coupled to (...) via a G protein.

The second messenger for the V₂ receptor is (...), which, via phosphorylation steps, directs the insertion of (...) in the luminal membranes.

The receptor for ADH on vascular smooth muscle is the (...) receptor, which is coupled to (...) via a G protein.

The second messenger for the V₁ receptor is (...), which produces (...) of vascular smooth muscle.

(...) is caused by failure of the posterior pituitary to secrete ADH; the collecting ducts are impermeable to water, and the urine cannot be concentrated.

Central diabetes insipidus is treated with an ADH analogue, (...).

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.

Nephrogenic diabetes insipidus is treated with (...).

In (...), excess ADH is secreted from an autonomous site, such as oat cell carcinoma of the lung.

SIADH is treated with an ADH antagonist such as (...) or water restriction.

(...) produces milk “letdown” or milk ejection from the lactating breast.

The major stimulus for oxytocin secretion is (...); however, (...) also cause milk letdown.

What are the major actions of oxytocin? (2)

Stimulation of powerful rhythmic contractions of uterine smooth muscle by oxytocin is the basis for its use in inducing (...) and in reducing (...).

The two active thyroid hormones are (...) and (...).

Thyroid hormones are synthesized by the (...) cells of the thyroid gland.

The material in the lumen of the follicles is (...), which is composed of newly synthesized thyroid hormones attached to (...).

(...), a glycoprotein containing large quantities of tyrosine, is synthesized on the rough endoplasmic reticulum and the Golgi apparatus of the thyroid follicular cells.

(...) is actively transported from blood into the thyroid follicular epithelial cells against both chemical and electrical gradients via (...).

The anions (...) block Na⁺-I⁻ cotransport into follicular cells and interfere with the synthesis of thyroid hormones.

Once I⁻ is pumped into the follicular epithelial cell, it is oxidized to (...) by the enzyme (...).

Thyroid peroxidase is inhibited by (...), which blocks the synthesis of thyroid hormones.

At the apical membrane, I₂ combines with the (...) moieties of TG, catalyzed by thyroid peroxidase, to form (...) and (...).

High levels of I⁻ inhibit organification and synthesis of thyroid hormones, which is known as the (...).

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 (...).

Iodinated TG is stored in the follicular lumen as (...) until the thyroid gland is stimulated to secrete its hormones (e.g., by TSH).

When the thyroid gland is stimulated, iodinated TG is (...) into the follicular epithelial cells.

(...) hydrolyze peptide bonds to release T₄, T₃, MIT, and DIT from TG.

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.

Most T₄ and T₃ circulates bound to (...); because only free thyroid hormones are physiologically active, this provides a reservoir of hormones.

In (...), blood levels of TBG decrease because there is decreased protein synthesis, resulting in a transient (...) in the level of free thyroid hormones.

During (...), high levels of estrogen inhibits hepatic breakdown of TBG, resulting in a transient (...) in the level of free thyroid hormones.

Circulating levels of TBG can be indirectly assessed with the (...), which measures the binding of radioactive T₃ to a synthetic resin.

The major secretory product of the thyroid gland is (...), which is the less active form of thyroid hormone.

In the target tissues, the enzyme (...) converts T₄ to T₃ by removing one atom of I₂ from the outer ring of the molecule.

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.

(...) inhibits 5′-iodinase in tissues such as skeletal muscle, thus lowering O₂ consumption and basal metabolic rate.

(...) acts on the thyrotrophs of the anterior pituitary to stimulate synthesis and secretion of TSH.

(...) regulates the growth of the thyroid gland (i.e. a trophic effect) and the secretion of thyroid hormones.

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.

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.

Activation of adenylyl cyclase generates (...), which serves as the second messenger for TSH.

The TSH receptor on the thyroid cells also is activated by (...), which are antibodies to the TSH receptor.

(...), a common form of hyperthyroidism, is caused by increased circulating levels of thyroid-stimulating immunoglobulins.

The first step in the action of thyroid hormones in target tissues is (...).

Once T₃ is produced inside the target cells, it binds to a (...).

The T3-receptor complex then binds to a (...) on DNA, where it stimulates (...).

A vast array of new proteins are synthesized under the direction of thyroid hormones, including (...).

What are the major effects of thyroid hormones? (5)

Thyroid hormones increase oxygen consumption in all tissues except (...) by inducing the synthesis and increasing the activity of (...).

The cardiac effects of thyroid hormones are explained by the fact that they induce the synthesis of (...).

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.

The most common form of hyperthyroidism is (...), an autoimmune disorder characterized by increased circulating levels of (...).

The diagnosis of hyperthyroidism is based on symptoms and measurement of increased levels of (...).

If the cause of hyperthyroidism is a disorder of the thyroid gland, then TSH levels will be (...).

If the cause of hyperthyroidism is a disorder of the hypothalamus or anterior pituitary, then TSH levels will be (...).

What are the symptoms of hyperthyroidism? (10)

Treatment of hyperthyroidism includes (...), which inhibits the synthesis of thyroid hormones, surgical removal of the gland, or radioactive ablation with (...)

The most common cause of hypothyroidism is (...) in which antibodies may either frankly destroy the gland or block thyroid hormone synthesis.

The diagnosis of hypothyroidism is based on symptoms and a finding of decreased levels of (...).

If the cause of hypothyroidism is a disorder of the thyroid gland, then TSH levels will be (...).

If the cause of hypothyroidism is a disorder of the hypothalamus or anterior pituitary, then TSH levels will be (...).

What are the symptoms of hypothyroidism? (10)

In some cases of hypothyroidism, (...) develops, in which there is edema due to accumulation of osmotically active mucopolysaccharides in interstitial fluid.

When the cause of hypothyroidism is a defect in the thyroid, a (...) develops from the unrelenting stimulation of the thyroid gland by TSH.

If hypothyroidism occurs in the perinatal period and is untreated, it results in an irreversible form of growth and mental retardation called (...).

Treatment of hypothyroidism involves thyroid hormone replacement therapy, usually (...).

Which of the following conditions are associated with goiter?

1. Graves disease
2. TSH-secreting tumors
3. factitious hyperthyroidism (ingestion of T₄)
4. autoimmune thyroiditis
5. TSH deficiency
6. I⁻ deficiency

The (...), which is in the inner zone of the adrenal gland that comprises 20% of the tissue, is of (...) origin and secretes (...).

The (...), which is in the outer zone of the adrenal gland that comprises 80% of the tissue, is of (...) origin and secretes (...).

The innermost zone of the adrenal cortex, called the (...), and the middle zone, called the (...), synthesize and secrete (...) and (...).

The outermost zone of the adrenal cortex, called the (...), secretes (...).

All of the steroids of the adrenal cortex are chemical modifications of a basic steroid nucleus, which is illustrated in the structure of (...).

The (...), represented by cortisol, have a ketone group at carbon 3 (C3) and hydroxyl groups at C11 and C21.

The (...), represented by aldosterone, have a double-bond oxygen at C18.

The (...), represented in the adrenal cortex by dehydroepiandrosterone (DHEA) and androstenedione, have a double-bond oxygen at C17.

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 (...).

The precursor for all adrenocortical steroids is (...).

The enzymes catalyzing the conversion of cholesterol to active steroid hormones require (...), molecular oxygen, and NADPH.

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.

The first step in the synthesis of all adrenocortical steroid hormones, conversion of cholesterol to pregnenolone, is catalyzed by (...).

Cholesterol desmolase, the rate-limiting enzyme in adrenocortical steroid hormone synthesis pathway, is stimulated by (...).

The major glucocorticoid produced in humans is (...), which is synthesized in the (...).

Cortisol is not the only steroid in the pathway with glucocorticoid activity; (...) is also a glucocorticoid.

(...) inhibits 11β-hydroxylase, the last step in cortisol synthesis.

(...) inhibits several steps in the pathway including cholesterol desmolase, the first step.

(...) are androgenic steroids produced in the (...).

Adrenal androgens have a ketone group at C17, thus they are also called (...).

The major mineralocorticoid in the body is (...), which is synthesized only in the (...).

The addition of the enzyme (...) in the zona glomerulosa allow the conversion of corticosterone to aldosterone.

Aldosterone is not the only steroid with mineralocorticoid activity; (...) and (...) also have mineralocorticoid activity.

The synthesis and secretion of steroid hormones by the adrenal cortex depend on the stimulation of cholesterol desmolase by (...).

The zonae fasciculata and reticularis, which secrete glucocorticoids and androgens, are under the exclusive control of the (...).

The zona glomerulosa, which secretes mineralocorticoids, depends on ACTH for the first step in steroid biosynthesis, but otherwise it is controlled via the (...).

An impressive feature of the regulation of cortisol secretion is its (...) nature and its (...) pattern.

The secretion of glucocorticoids by the zonae fasciculata/reticularis is regulated exclusively by the (...).

(...) acts on the corticotrophs by an adenylyl cyclase/cAMP mechanism to cause secretion of ACTH into the bloodstream.

(...) activates cholesterol desmolase in the adrenal cortex and up-regulates transcrption of its own receptor.

ACTH has a (...) secretory pattern that drives a parallel pattern of cortisol secretion.

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 (...).

The (...) test is based on the negative feedback effects of cortisol on the CRH-ACTH axis.

When a low dose of dexamethasone is given to a healthy person, it inhibits (...).

The major use of the dexamethasone suppression test is in persons with (...).

If the cause of hypercortisolism is (...), a low dose of dexamethasone does not suppress cortisol secretion but a high dose of dexamethasone does.

If the cause of hypercortisolism is an (...), then neither low-dose nor high-dose dexamethasone suppresses cortisol secretion.

The major con­trol of aldosterone secretion is via the (...).

The mediator of mineralcorticoid secretion is (...), which increases the synthesis and secretion of aldosterone by stimulating cholesterol desmolase and aldosterone synthase.

(...) is the enzyme that catalyzes the conversion of angiotensinogen to angiotensin I, which is inactive.

(...) catalyzes the conversion of angiotensin I to angiotensin II, which then acts on the zona glomerulosa to stimulate aldosterone synthesis.

Increases in serum (...) concentration increase aldosterone secretion.

What are the major actions of glucocorticoids? (7)

Glucocorticoids are essential for survival during (...) because they stimulate these gluconeogenic routes.

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.

Aldosterone has three actions on the late distal tubule and collecting ducts:

1. It increases (...) reabsorption.
2. It increases (...) secretion.
3. It increases (...) secretion.

Renal cells contain the enzyme (...), which converts high-affinity cortisol to low affinity cortisone to prevent it from dominating mineralocorticoid receptors.

In (...), there is increased synthesis of adrenal androgens leading to masculinization in females and suppression of gonadal function in both males and females.

In the adrenogenital syndromes, due to the overproduction of adrenal androgens, there will be increased urinary levels of (...).

Cortisol promotes gluconeogenesis; therefore, excess levels produce (...) and deficits produce (...) upon fasting.

Aldosterone causes increased K⁺ secretion by the renal principal cells; thus excess causes (...) and deficiency causes (...).

Because adrenal androgens have testosterone-like effects, in females, overproduction causes (...) and deficits result in (...).

(...) is commonly caused by autoimmune destruction of all zones of the adrenal cortex, resulting in decreased synthesis of all adrenocortical hormones.

Addison disease also is characterized by (...), particularly of the elbows, knees, nail beds, nipples, and areolae and on recent scars.

Hyperpigmentation in Addison disease is a result of increased levels of (...).

Conditions of (...) occur when there is insufficient CRH or insufficient ACTH.

(...) is the result of chronic excess of glucocorticoids due to overproduction by the adrenal cortex or exogenous administration.

(...) is characterized by excess glucocorticoids, in which the cause is hypersecretion of ACTH from a pituitary adenoma.

What are the symptoms of Cushing syndrome? (8)

The (...), in which a synthetic glucocorticoid is administered, can distinguish between Cushing syndrome and Cushing disease.

In (...), because the tumor functions autonomously, cortisol secretion is not suppressed by either low- or high-dose dexamethasone.

In (...), ACTH and cortisol secretion are suppressed by high-dose dexamethasone but not by low-dose dexamethasone.

Treatment of Cushing syndrome includes administration of drugs such as (...), which block steroid hormone biosynthesis.

Because of its different etiology, treatment of Cushing disease involves (...).

(...) is caused by an aldosterone-secreting tumor.

Treatment of Conn syndrome consists of administration of an aldosterone antagonist such as (...), followed by surgical removal of the tumor.

The most common enzymatic defect in the steroid hormone biosynthetic pathways is deficiency of (...), which belongs to a group of disorders called (...).

Without 21β-hydroxylase, the adrenal cortex is unable to convert progesterone to (...) or 17-hydroxyprogesterone to (...).

In 21β-hydroxylase deficiency, steroid intermediates will accumulate above the enzyme block and be shunted toward production of (...).

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 (...).

A less common congenital abnormality of the steroid hormone biosynthetic pathway is deficiency of (...).

Without 17α-hydroxylase, pregnenolone cannot be converted to (...) and progesterone cannot be converted to (...).

In this 17α-hydroxylase deficiency, steroid intermediates accumulate to the left of the enzyme block and will be shunted toward production of (...).

The endocrine cells of the pancreas are arranged in clusters called the (...), which compose 1% to 2% of the pancreatic mass.

The β cells compose 65% of the islet and secrete (...).

The α cells compose 20% of the islet and secrete (...).

The delta (δ) cells compose 10% of the islet and secrete (...).

The remaining cells of the pancreatic islets secrete (...).

Insulin is synthesized and secreted by the (...).

Insulin is a peptide hormone consisting of two straight chains designated as the (...) and (...).

The synthesis of insulin is directed by a gene on (...), a member of a superfamily of genes that encode related growth factors.

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).

The signal peptide is cleaved from preproinsulin early in the biosynthetic process, yielding (...)

Proinsulin is packaged in secretory granules on the Golgi apparatus, during which, proteases cleave the connecting peptide, yielding (...).

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.

The most important factor influencing the secretion of insulin by β cells is (...)

The β cell membrane contains (...), a specific transporter for glucose that moves glucose from the blood into the cell by facilitated diffusion

Once inside the cell, glucose is phosphorylated to glucose-6-phosphate by (...), and glucose-6-phosphate is subsequently oxidized.

Oxidation of glucose-6-phosphate generates (...), which appears to be the key factor that regulates insulin secretion.

When ATP levels inside the β cell increase, the ATP-sensitive (...) channels close, which depolarizes the β cell membrane.

The depolarization of the β cell caused by closure of the K⁺ channels opens voltage-sensitive (...) channels.

Increases in intracellular Ca²⁺ concentration within the β cell causes exocytosis of the (...)-containing secretory granules

Oral glucose is a more powerful stimulant for insulin secretion than intravenous glucose because it stimulates the secretion of (...).

(...) activates a G_q protein coupled to phospholipase C, which leads to a rise in intracellular Ca²⁺, causing exocytosis of insulin.

(...) inhibits the insulin-releasing mechanism that glucagon stimulates.

(...) treat type II diabetes mellitus by stimulating insulin release from β cells by closing the ATP-dependent K⁺ channels.

The insulin receptor is a tetramer composed of two (...) and two (...), joined by disulfide bonds.

The (...) of the insulin receptor have intrinsic tyrosine kinase activity.

Insulin binds to the (...) of the tetrameric insulin receptor, producing a conformational change in the receptor.

The conformational change in the α subunits of the insulin receptor activates tyrosine kinase in the β subunits, which (...) presence of ATP.

Activated (...) on the β subunits phosphorylates several other proteins or enzymes that are involved in the physiologic actions of insulin.

Insulin (...) its own receptor by decreasing the rate of synthesis and increasing the rate of degradation of the receptor.

What are the major actions of insulin? (4)

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 (...).

Insulin also appears to have a direct effect on the hypothalamic (...) center independent of the changes it produces in blood glucose concentration.

(...) is caused by destruction of β cells, often as a result of an autoimmune process.

The increased levels of ketoacids in type I diabetes mellitus cause a form of metabolic acidosis called (...).

In diabetes mellitus, the nonreabsorbed glucose in the renal tubules acts as an osmotic solute in urine, producing (...).

(...) is often associated with obesity and is caused by down-regulation of insulin receptors in target tissues and insulin resistance.

(...) can be used to treat type II diabetes mellitus by stimulating pancreatic insulin secretion, while (...) up-regulate insulin receptors on target tissues.

Glucagon is synthesized and secreted by the (...) of the islets of Langerhans.

The major factor stimulating the secretion of glucagon is (...).

Glucagon secretion also is stimulated by the ingestion of protein, specifically by the amino acids (...) and (...).

Another factor stimulating glucagon secretion is (...), which is secreted from the gastrointestinal tract when protein or fat is ingested.

The glucagon receptor is coupled to (...) via a G protein and second messenger is (...).

What are the major actions of glucagon? (2)

Glucagon increases the blood glucose concentration by (1) stimulating (...) and inhibiting (...); and (2) by increasing gluconeogenesis by decreasing the production of (...).

Pancreatic somatostatin is secreted by the (...) of the islets of Langerhans.

Pancreatic somatostatin inhibits secretion of (...) via paracrine actions.

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.

(...) is a decrease in the plasma Ca²⁺ concentration, which produces symptoms of hyperreflexia, spontaneous twitching, muscle cramps, and tingling and numbness.

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.

(...) is an increase in the plasma Ca²⁺ concentration, which produces symptoms of constipation, polyuria, polydipsia, hyporeflexia, lethargy, coma, and death.

Changes in plasma (...) concentration alter the total Ca²⁺ concentration in the same direction.

Changes in plasma (...) concentration alter the ionized Ca²⁺ concentration by changing the fraction of complexed Ca²⁺.

(...) abnormalities alter the ionized Ca²⁺ concentration by changing the fraction of Ca²⁺ bound to plasma albumin.

In (...), there is more H⁺ in blood to bind to albumin, leaving fewer sites for Ca²⁺ to bind, thus the free ionized Ca²⁺ concentration (...).

In (...), there is less H⁺ in blood to bind to albumin, leaving more sites for Ca²⁺ to bind, thus the free ionized Ca²⁺ concentration (...).

What three organ systems are involved in Ca²⁺ homeostasis?

The (...) of the parathyroid glands synthesize and secrete PTH.

PTH secretion is regulated by plasma (...) concentration; when it decreases to less than (...), PTH secretion is stimulated.

The parathyroid cell membrane contains (...) that are linked, via a G protein to phospholipase C.

Chronic (...) causes (...), which is characterized by increased synthesis and storage of PTH and hyperplasia of the parathyroid glands.

Chronic (...) causes decreased synthesis and storage of PTH, increased breakdown of stored PTH, and release of inactive PTH fragments into the circulation.

(...) has parallel, although less important, effects on PTH secretion as Ca²⁺.

The receptor for PTH is coupled, via a G protein, to (...).

In bone, PTH receptors are located only on (...).

Initially and transiently, PTH causes (...) by a direct action on osteoblasts.

In a second, long-lasting, indirect action on osteoclasts, PTH causes (...), mediated by (...) released from osteoblasts.

PTH inhibits (...) reabsorption in the proximal convoluted tubule.

The cAMP generated in cells of the proximal tubule is excreted in urine and is called (...).

The phosphaturic action of PTH is critical because otherwise the phosphate resorbed from bone would (...).

PTH stimulates (...) reabsorption in the proximal convoluted tubule.

PTH does not have direct actions on the small intestine, although indirectly it stimulates intestinal Ca²⁺ absorption via (...).

Primary hyperparathyroidism is most commonly caused by (...).

In primary hyperparathyroidism, (...) results from increased bone re­­sorption, increased renal Ca²⁺ reabsorption, and increased intestinal Ca²⁺ absorption.

In primary hyperparathyroidism, (...) results from decreased renal phosphate reabsorption and phosphaturia.

Persons with primary hyperparathyroidism are said to have "(...)."

In secondary hyperparathyroidism, the parathyroid glands are stimulated to secrete excessive PTH secondary to (...), which can be caused by (...).

(...) is a relatively common, inadvertent consequence of thyroid surgery or parathyroid surgery.

In hypoparathyroidism, (...) results from decreased bone resorption, decreased renal Ca²⁺ reabsorption, and decreased intestinal Ca²⁺ absorption.

In hypoparathyroidism, (...) results from increased phosphate reabsorption.

Patients with (...) have hypocalcemia and hyperphosphatemia; however, circulating levels of PTH are increased rather than decreased.

Pseudohypoparathyroidism is an inherited autosomal dominant disorder in which the (...) for PTH in kidney and bone is defective.

Some malignant tumors secrete (...), which is structurally homologous with the PTH secreted by the parathyroid glands, with all the same physiologic actions.

Humoral hypercalcemia of malignancy is treated with (...), which inhibits renal Ca²⁺ reabsorption, and inhibitors of bone resorption such as (...).

(...) is an autosomal dominant disorder characterized by decreased urinary Ca²⁺ excretion and increased serum Ca²⁺ concentration.

FHH is caused by inactivating mutations of (...) in the parathyroid glands and the thick, ascending limb of the kidney.

Calcitonin is synthesized and secreted by the (...) of the thyroid gland.

The major stimulus for calcitonin secretion is (...).

The major action of calcitonin is to (...), which decreases the plasma Ca²⁺ concentration.

(...) in conjunction with PTH, is the second major regulatory hormone for Ca²⁺ and phosphate metabolism.

Vitamin D in the form of (...) is provided in the diet and is produced in the skin from cholesterol.

Cholecalciferol is physiologically inactive; it is hydroxylated in the liver to form (...), which also is inactive.

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.

C1 hydroxylation of 25-hydroxycholecalciferol in the kidney is catalyzed by the enzyme (...).

1α-hydroxylase activity is stimulated by(1) decreased plasma (...) concentration, (2) increased circulating levels of (...), and (3) decreased plasma (...) concentration.

The overall role of 1,25-dihydroxycholecalciferol is to increase the plasma concentration of (...) to promote (...).

In the intestine, 1,25-dihydroxycholecalciferol induces the synthesis of a vitamin D–dependent Ca2+-binding protein called (...).

The actions of 1,25-dihydroxycholecalciferol on the kidney are parallel to its actions on the intestine—it stimulates (...).

In bone, 1,25-dihydroxycholecalciferol acts synergistically with PTH to stimulate (...).

In children, vitamin D deficiency causes (...), a condition in which insufficient amounts of Ca²⁺ and phosphate are available to mineralize the growing bones.

In adults, vitamin D deficiency results in (...), in which new bone fails to mineralize, resulting in bending and softening of the weight-bearing bones.

(...) occurs when the kidney is unable to produce the active metabolite, 1,25-dihydroxycholecalciferol.

Vitamin D resistance can be caused by the congenital absence of 1α-hydroxylase or, more commonly, by (...).