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<database>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>a multiple choice question:</question>
<multiple_choice>
<choice>a</choice>
<choice>b</choice>
<choice>c</choice>
<choice>d</choice>
<choice>e</choice>
</multiple_choice>
<answer>a</answer>
<resources></resources>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>Name all major hormones produced by the anterior pituitary.</question>
<answer>GH, prolactin, TSH, LH, FSH, ACTH</answer>
<type>review</type>
<resources>BRS 2nd edition: p. 248</resources>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What two hormones is GH (somatotropin) homologous to?</question>
<answer>Prolactin and human plancetal lactogen.</answer>
<resources></resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What increases secretion of GH?</question>
<answer>GH secretion is increased by starvation, hypoglycemia, hormones related to puberty, stress, exercise and sleeping</answer>
<resources></resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What decreases GH secretion?</question>
<answer>Somatostatin, somatomedins, obesity, hyperglycemia and pregnancy decrease GH secretion</answer>
<resources>BRS 2nd ed.: p. 249</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What does GNRH do?</question>
<answer>GNRH stimulates synthesis and secretion of GH.</answer>
<resources>BRS 2nd: 249</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>How does somatostatin inhibit secretion of GH</question>
<answer>Somatostatin inhibits secretion of GH by blocking the response of the anterior pituitary to GHRH</answer>
<resources>BRS2nd: 249</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>Describe the negative feedback systems acting to downregulate GH.</question>
<answer>1) Somatomedins, produced by GH target tissues, inhibit secretion of GH by acting directly on the anterior pituitary and by stimulating secretion of somatostatin from the hypothalmus.2) GHRH inhibits its own secretion from the hypothalamus.3) GH inhibits its own secretion by stimulating secretion of stamtostatins from hypothalamus.</answer>
<resources>BRS2nd: p. 249</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What are the direct actions of GH?</question>
<answer>1) decrease gluocse update into cells (daibaetogenic) 2) increase lipolysis 3) increase protein synthesis in muscle and increase lean body mass 4) increase production of IGF</answer>
<resources>BRS2nd: p. 250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What is IGF? Where is it produced? What are its effects?</question>
<answer>IGF, insulin-like growth factors, are somatomedins produced by the liver. The direct effects IGF include: (1) incrase in protein synthesis in chnodroctyes (2) increase in linear growth (pubertal growth spurt) (3) increase in protein synthesis in muscle and increase in lean body mass (3) increase in protein sythesis in most organs and increase in organ size.</answer>
<resources>BRS2nd: p. 250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What are the effects of GH deficiency?</question>
<answer>GH deficiency in children causes failure to grow, short stature, mild obesity and delayed puberty.</answer>
<resources>BRS2nd: p.250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What are the causes of GH deficency?</question>
<answer>(1) Lack of anterior pituitary GH(2) Hypothalmic dysfunction with corresponding decrease in GHRH(3) Failure to generate IGF in liver(4) GH receptor deficiency</answer>
<resources>BRS2nd: p. 250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>How is GH excess treated? What are the effects of GH excess before and after puberty?</question>
<answer>GH excess can be treated with somatostatin analogs (e.g. octreotide).Before puberty, excess GH causes increased linear growth (gigantism).After puberty, excess GH causes incrased periosteal bone growth, increased organ size and glucose intolerance.</answer>
<resources>BRS2nd: p. 250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What causes acromegaly, what are its symptoms, and what are it's most serious health consequences?</question>
<answer>Acromegaly is a hormonal disorder that results when the pituitary gland produces excess growth hormone (GH). The name acromegaly comes from the Greek words for "extremities" and "enlargement" and reflects one of its most common symptoms, the abnormal growth of the hands and feet. Soft tissue swelling of the hands and feet is often an early feature, with patients noticing a change in ring or shoe size. Gradually, bony changes alter the patient's facial features: the brow and lower jaw protrude, the nasal bone enlarges, and spacing of the teeth increases.The most serious health consequences of acromegaly are diabetes mellitus, hypertension, and increased risk of cardiovascular disease. Patients with acromegaly are also at increased risk for polyps of the colon that can develop into cancer.</answer>
<resources>http://www.endocrine.niddk.nih.gov/pubs/acro/a</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>How does the hypothalmus regulate prolactin secretion by the anterior pituitary?</question>
<answer>Prolactin secretion is tonically inhibited by dopamine which is secreted by the hypothalamus.Prolactin secretion is increased by thyrotropin-releasing hormone (TRH) secreated by the hypothalamus.</answer>
<resources>BRS2nd: p. 250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What causes the hypothalamus to relase dopamine?</question>
<answer>A negative feedback systems exists in which prolactin stimulates the hypothalamus to release dopamine.</answer>
<resources>BRS2nd: p. 250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What are the actions of prolactin?</question>
<answer>(1) Stiumulates milk produciton (2) Stimulates breast development (in supportive role with estrogen) (3) Inhibits ovulation by decreasing synthesis and release of GnRH (4) Inhibits spermatogenesis by decreasing GnRH.</answer>
<resources>BRS2nd: p. 250</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What does prolactin deficiency result in?</question>
<answer>Failure to lactate.</answer>
<resources>BRS2nd: p. 251</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>anterior pituitary</keywords>
<difficulty>1</difficulty>
<question>What causes prolactin excess, what does it result in and how is it treated?</question>
<answer>Prolactin excess is caused by hypothalmic destruction due to loss of tonic inhibitory control by dopamine or from prlactinomas. This causes galactorrhea and ecreased libido, failure to ovulate and amenorrhea (GnRH secretion inhibited). This is treated with bromocriptine, which acts as a dopamine agonist.</answer>
<resources>BRS2nd: p. 251</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>posterior pituitary</keywords>
<difficulty>1</difficulty>
<question>Where is ADH produced and what does it do?</question>
<answer>ADH originates primarily in the supraoptic nuclei of the hypothalmus. It regulates serum osmolarity by increase water permeability of the late distal tubules and collecting ducts.</answer>
<resources>BRS2nd: p. 252</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>posterior pituitary, ADH</keywords>
<difficulty>1</difficulty>
<question>What factors increase ADH secretion?</question>
<answer>(1) increase in serum osmolality, (2) volume contraction (3) pain (4) nausea (5) hypoglycemia (6) nicotine, opiates and antineoplastic drugs</answer>
<resources>BRS2nd: p. 252</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>posterior pituitary, ADH</keywords>
<difficulty>1</difficulty>
<question>What factors decrease ADH secretion?</question>
<answer>(1) decrease in serum osmolality, (2) ethanol (3) alpha-agonists (4) ANF</answer>
<resources>BRS2nd: p. 252</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>posterior pituitary, oxytocin</keywords>
<difficulty>1</difficulty>
<question>Where is oxytocin produced and what does it do?</question>
<answer>Oxytocin primarily originates in the paraventricular nuclei of the hypothalamus. It causes ejection of milk from the breast when stimulated by suckling.</answer>
<resources>BRS2nd: p. 252</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>posterior pituitary, oxytocin</keywords>
<difficulty>1</difficulty>
<question>What causes oxytocin secretion?</question>
<answer>Suckling is the major stimulus, whereby afferent fibers carry impulses from the nipple to the spinal cord resulting in release of oxytocin from posterior pituitary. Additionaly sight or sound of infant may stimulate release even in absence of suckling. Lastly, dilation of cervix and orgasm increase oxytocin secretion.</answer>
<resources>BRS2nd: p. 252</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>posterior pituitary, oxytocin</keywords>
<difficulty>1</difficulty>
<question>What are the actions of oxytocin?</question>
<answer>Oxytocin causes:(1) contraction of myoepithelial cells forcing mil from mamary alveoli into ducts,(2) contraction of the uterus: during pregnancy, oxytocin receptors in uterus upregulated as parturition approaches. Thus oxytocin can be used to induce labor. and reduce postpartum bleeding.</answer>
<resources>BRS2nd: p. 253</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>Describe the pathway through which I- is converted into T3 and T4.</question>
<answer>1) I- is actively transported into thyroid follicular cells.&lt;br/&gt;2) I- is then oxidized to I2. This is catalyzed by peroxidase.&lt;br/&gt;3) On the borders of the follicular epithelia and lumen, I2 reacts with thyroglobulin to form monoiodotyrosine (MIT) and diiodotyrosine (DIT).&lt;br/&gt;4) Two DITs combine to form thyroxine (T4). DIT and MIT combine to form thyronine (T3).</answer>
<resources>BRS2nd: p. 253-54</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What is the Wolff-Chaikoff effect (thyroid-related)?</question>
<answer>High levels of I- in the blood inhibit the I- pump. Less I- enters thyroid follicular cells and thyroid hormone synthesis is inhibited.</answer>
<resources>BRS2nd: p. 253</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>The peroxidase enzyme is active in several reactions of the thryoid hormone pathway. Which reactions do these include? What drug is used to inhibit this enzyme therapeutically?</question>
<answer>The peroxidase enzyme catalyzes the reactions:&lt;br/&gt;1) 2I- -->I2&lt;br/&gt;2) I2 + tyrosine -->MIT, DIT&lt;br/&gt;3) MIT + DIT -->T3 and 2DIT -->T4&lt;br/&gt;The peroxidase enzyme is inhibited by propylthiouracil.&lt;br/&gt;</answer>
<resources>BRS2nd: p. 253</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What happens at the biochemical level when the thyroid gland is stimulated by TSH? In other words, what is the process through which T3 and T4 is released into the blood?</question>
<answer>When thyroid cells are stimulated by TSH, iodinated thryoglobulin must e taken back into the follicular cells from the lumen (where it's stored). Lysosomal enzymes digest the thryoglobulins and relases T4 and T3 into circulation.</answer>
<resources>BRS2nd: p. 254</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What is thyroid deiodinase and what are the consequenes of deficiency of this enzyme?</question>
<answer>MIT and DIT are deiodinated by thyroid deiodinase. The I2 is released as free I2 into the blood (?). A deficiency in this enzyme causes a buildup of MIT and DIT and reduces the free I2 pool simulating a general I2 deficiency.</answer>
<resources>BRS2nd: p. 254</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What consequence does hepatic failure have of the free thryoid hormone concentrations in the blood? What effect does pregnancy have?</question>
<answer>In circulation, T3 and T4 are bound to thyroxine-binding globulin (TBG). If liver failure, TBG levels decrease, free TH levels increase. In pregancy, TBG levels increase and free TH levels decrease.</answer>
<resources>BRS2nd: p. 254</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>Through what regulatory pathway are thyroid hormones synthesized and released into circulation?</question>
<answer>TRH made by the hypothalamus acts on the anterior pituitary which in response releases TSH. TSH increases both synthesis and secretion by thyroid follicular cells of thyroid hormones.</answer>
<resources>BRS2nd: p. 255</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>Through what pathway are thyroid hormones downregulated?</question>
<answer>T3 down-regulates TRH receptores in the anterior pitutitary, inhibiting TSH secretion and reducing thyroid hormone synthesis and secretion.</answer>
<resources>BRS2nd: p. 255</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What causes the high circulating levels of htyroid hormones found in patients with Graves' disease?</question>
<answer>Thyroid-stimulating immunoglobulins are antiboides to the TSH receptors on the thyroid gland. In Graves' disease, these circulate in high concentrations leading to high circulating levels of thyroid hormone and low concentrations of TSH (due to feedback inhibition).</answer>
<resources>BRS2nd: p. 255</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>T/F: T4 is three to four times more potent than T3</question>
<answer>False: T3 is three to four times more potent than T4.</answer>
<resources>BRS2nd: p. 255</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>How does thyroid hormone affect bone formation and growth?</question>
<answer>Thryoid hormones act with GH and somatomedins to promone bone formation. TH stimulates bone maturation  as a result of ossification of the growth plates. Note that in TH deficiency, bone age is less than chronologic age.</answer>
<resources>BRS2nd: p. 256</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What role does thyroid hormone play in development?</question>
<answer>Maturation of the CNS is dependent on thyroid hormone in the perinatal period. Deficiency at this time causes irreversible mental retardation.</answer>
<resources>BRS2nd: p. 256</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What are the symptoms of hyperthyroidism?</question>
<answer>1) Increased metabolic rate&lt;br/&gt;2) Weight loss&lt;br/&gt;3) Negative nitrogen balance&lt;br/&gt;4) Increased heat production (sweating)&lt;br/&gt;5) Increased cardiac output&lt;br/&gt;6) Dyspnea&lt;br/&gt;7) Tremor, weakness&lt;br/&gt;8) Exophthalmos&lt;br/&gt;9) Goiter</answer>
<resources>BRS2nd: p. 257</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What are the symptoms of hypothyroidism?</question>
<answer>1) decreased metabolic weight&lt;br/&gt;2) weight gain&lt;br/&gt;3) Positive nitrogen balance&lt;br/&gt;4) decreased heat production&lt;br/&gt;5) decreased cardiac output&lt;br/&gt;6) hypoventilation&lt;br/&gt;7) lethargy, mental slowness&lt;br/&gt;8) drooping eyelids&lt;br/&gt;9) myxedema&lt;br/&gt;10) Growth and mental retardation (perinatal)&lt;br/&gt;11) Goiter&lt;br/&gt;</answer>
<resources>BRS2nd: p. 257</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What effects does thyroid hormone have on BMR?</question>
<answer>TH increases O2 consumption and rasies BMR in all tissues except the brain, spleen and gonads. It also increases synthesis of Na,K-ATPase.</answer>
<resources>BRS2nd: p. 256</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>How does thyroid hormone affect the cardiovascular and respiratory systems?</question>
<answer>TH acts to increase cardiac output and the ventilaiton rate to ensure that more O2 is delivered to tissues.</answer>
<resources>BRS2nd: p. 256</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"thyroid gland"</keywords>
<difficulty>1</difficulty>
<question>What metabolic effects does thyroid hormone have?</question>
<answer>1) Increased absorption of glucose in GI tract&lt;br/&gt;2) Glycogenolysis, gluconeogenesis, and gloucse oxidation are increased.3) Lipolysis increased.4) Protein synthesis and degradation are increased, overall effect is catabolic.5) Cholesterol synthesis and degradation.</answer>
<resources>BRS2nd: p. 256</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What are the three zones of the adrenal cortex and what does each zone produce?</question>
<answer>1) zona glomerulosa: aldosterone&lt;br/&gt;2) zona fasiculata: glucocorticoids&lt;br/&gt;3) zona reticularis: androgens&lt;br/&gt;</answer>
<resources>BRS2nd: p. 257</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>Which steroids make up the 21 carbon group?</question>
<answer>Progeresterone, deoxycorticosterone, aldosterone and cortisol.</answer>
<resources>BRS2nd: p. 257</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What is the precursor to all steroids?</question>
<answer>Cholesterol.</answer>
<resources>BRS2nd: p. 257</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What steroids are in the 19-carbon group and what type of activity do these steroids have?</question>
<answer>19-carbon steroids have androgenic activity and include dehydroepiandrosterone and androstenedione.</answer>
<resources>BRS2nd: p. 257-8</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What type of activity do the 18-carbon steroids have? What are their immediate precursors and where are they converted to their final state?</question>
<answer>18 carbon steroids have estrogenic activty. The 19-carbon precursors are aromatized to produce estrogens in the ovaries and placenta.</answer>
<resources>BRS2nd: p. 258</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>When are glucocorticoid elvels highest and lowest?</question>
<answer>Cortisol secretion oscillates with a 24-hour periodicity. For nightsleepers, cortisol levels are highest just before waking and lowest around midnight.</answer>
<resources>BRS2nd: p. 258</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>Describe the pathway up to ACTH secretion for the secretion of glucocorticoids.</question>
<answer>The paraventricular nuclei of the hypothalamus reluease CRH into the hypothalmic-hypophysical portal system and bind to CRH receptors on corticotrophs of the anterior pituitatary. This leads to synthesis of POMC which is is converted to ACTH and secreted.</answer>
<resources>BRS2nd: p. 258</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>How does ACTH work in to increase steroid synthesis and secretion?</question>
<answer>1) ACTH increases steroid hormone synthesis in all zones of the adrenal cortex by stimulating cholesterol desmolase and increaseing conversion of cholesterol to pregnenolone.&lt;br/&gt;2) ACTH up-regulates its own receptor so that sensitivity of the adrental cortex to ACTH is increased.</answer>
<resources>BRS2nd: p. 258</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>How is cortisol downregulated?</question>
<answer>Through a negative feedback loop, cortisol inhibts secretion of CRH and ACTH.</answer>
<resources>BRS2nd: p. 259</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What is the dexamethasone suppression test?</question>
<answer>Dexamethasone, a potent glucocorticoid, inhibits release of ACTH via negative feedback. If patient is normal, dex inhibits release of ACTH and cortisol.</answer>
<resources>BRS2nd: p. 259</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>How does the renin-angiotensin-aldosterone system lead to secretion of aldosterone?</question>
<answer>Decreases in blood volume cause an increase in renin secretion. Renin converts angiotensinogen to angiotensin I which is converted to angiotensin II by ACE. Angiotensin II acts on the zona glomerulosa to increase the conversion of corticosterone to aldosterone.</answer>
<resources>BRS2nd: p. 260</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>How do glucosteroids stimulate gluconeogenesis?</question>
<answer>1) Increase protein catabolism in muscle and decrease protein synthesis -->provides more amino acids to liver for gluconeogenesis.&lt;br/&gt;2) Decrease glucose utilization and insulin sensitivity of adipose tissue.&lt;br/&gt;3) Increase lipolysis -->provides more glycerol for gluconeogenesis.</answer>
<resources>BRS2nd: p. 261</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What are the anti-inflammatory effects of glucocorticoids?</question>
<answer>1) Induce the synthesis of lipocortin which in turn (through several steps) inhibits the release of arachidonate, the precursor for prostaglandins and leukotriene synthesis.&lt;br/&gt;2) Inhibit produciton of IL-2 and inhibit proliferation of T lymphocytes.&lt;br/&gt;3) Inhibt release of histamine and serotonin from mast cells and platelets.</answer>
<resources>BRS2nd: p. 261</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>Why does cortisol deficiency cause blood pressure to decrease?</question>
<answer>Glucocorticoids are required for the vasoconstrictor effect of norepinephrine on the arterioles. Without it, blood pressure decreases.</answer>
<resources>BRS2nd: p. 261</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex" ald</keywords>
<difficulty>1</difficulty>
<question>What are the actions of mineralocorticoids (aldosterone)?</question>
<answer>1) Increase in renal Na+ absorption (principal cells of late distal tubule and CCD)&lt;br/&gt;2) Increase in renal K+ secretion (principal cells of late distal tubule and CCD)&lt;br/&gt;3) Increase in renal H+ secretion (alpha-intercalated cells of late distal tubule and CCD)&lt;br/&gt;</answer>
<resources>BRS2nd: p. 261</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex" "Ad</keywords>
<difficulty>1</difficulty>
<question>What is Addison's disease and what are the assoicated clinical features? How are ACTH levels affected? How is it treated?</question>
<answer>Addison's disease is a primary adrenocortical insufficiency and results in a decrease in glucocorticoid,s androgens and mineralocorticoids.&lt;br/&gt;1) Symptoms:&lt;br/&gt;a) Hypoglycemia (caused by cortisol deficiency)&lt;br/&gt;b) weight loss, nausea, weakness&lt;br/&gt;c) hypotension, hyperkalemia, metabolic acidosis (aldosterone insufficiency)&lt;br/&gt;d) decreased pubic and axillary hair in women,e) hyperpigmentation (caused by increase in ACTH which contains MSH fragment).2) ACTH levels are increased due to negative feedback of decreased cortisol.3) Replacement of glucocorticoids and mineralocorticoids.</answer>
<resources>BRS2nd: p. 262-3</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What is secondary adrenocortical insufficiency and how can you distinguish it from Addison's disease?</question>
<answer>In secondary adrenocortical insufficency, there is a deficiency of ACTH. Neither hyperpigmentation nor hyperkalemia, metabolic acidosis or volume contraction are observed. The remainder of the symptoms are the same as Addison's disease.</answer>
<resources>BRS2nd: p. 263</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What is Cushing's syndrome? What are it's symptoms?</question>
<answer>Cushing's syndrom is an excess of ACTH.&lt;br/&gt;Symptomes include:&lt;br/&gt;1) Increase in cortisol and androgen levels.&lt;br/&gt;2) Hyperglycemia (caused by elevated cortisol levels)&lt;br/&gt;3) Increase in protein catabolism and muscle wasting&lt;br/&gt;4) Central obesity (round face, supraclavicular fat)&lt;br/&gt;5) Poor wound healing&lt;br/&gt;6) Virilization of women (caused by elevated levels of adrenal androgens)&lt;br/&gt;7) Hypertension (elevated levels of cortisol and aldosterone)&lt;br/&gt;8) Osteoporosis (elevated coritsol levels cause increased bone resorption)&lt;br/&gt;9) Striae&lt;br/&gt;</answer>
<resources>BRS2nd: p. 263</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What causes hyperaldosteronism (Conn's Syndrome) and what are it's symptoms?</question>
<answer>Hyperaldosteronism is caused by an aldosterone secreteing tumor and is characterized by:&lt;br/&gt;1) Hypertension (aldosterone increases Na+ reabsorption -->increase blood volume)&lt;br/&gt;2) Hypokalemia (aldosteron increases K+ secretion)&lt;br/&gt;3) Metabolic alkalosis (aldosterone increases H+ secretion)&lt;br/&gt;4) decrease in renin secretion (increased blood volume and pressure inhibit renin secretion by negative freedback)</answer>
<resources>BRS2nd: p. 264</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What are the symptoms of 21beta-hydroxylase deficiency?</question>
<answer>1) Decrease in cortisol and aldosterone levels (the enzyme deficiency happens upstream in the synthesis of these steroids)&lt;br/&gt;2) Decrease in 17-hydroxyprogesterone and progesteron levels (increased concentration of intermediates downstream negatively feedback and block continued synthesis)&lt;br/&gt;3) Increased ACTH (due to decreased feedback inhibition by cortisol)&lt;br/&gt;4) Hyperplasia of zona fasciculata and zona reticularis (due to high levels of of ACTH)&lt;br/&gt;5) Increase in adrenal androgens (due to increase in precursors)&lt;br/&gt;6) Virilization in women&lt;br/&gt;7) Early acceleration of linear growhth and early appearance of pubic and axillary hair&lt;br/&gt;8) Suppression of gonadal function in men and women</answer>
<resources>BRS2nd: p. 264</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"adrenal gland" "adrenal cortex"</keywords>
<difficulty>1</difficulty>
<question>What characterizes 17alpha-hydroxylase deficiency?</question>
<answer>1) Decreased androgen and glucocorticoid levels (upstream precursors aren't made)&lt;br/&gt;2) Increased aldosterone levels (intermediats accumulate to left of enzyme block and are shunted toward production of mineralocorticoids)&lt;br/&gt;3) Lack of pubic anx axillary hair in women&lt;br/&gt;4) Hypoglycemia (due to decreased glucocorticoids)&lt;br/&gt;5) Metabolic alkylosis, hypokalemia and hyypertension (due to increased aldosterone)&lt;br/&gt;6) Increased ACTH (due to decreaesd cortisol)</answer>
<resources>BRS2nd: p. 264</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What type of messenger system is associated with insulin and with glucagon?</question>
<answer>Insulin: tyrosine kinase recepter&lt;br/&gt;Glucagon: cAMP mechanism</answer>
<resources>BRS2nd: p. 265</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What is the major stimulus for the secretion of glucagon?</question>
<answer>Decreased blood glucose stimulates glucagon secretion.</answer>
<resources>BRS2nd: p. 265</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What are the primary actions of glucagon?</question>
<answer>1) Increases glycogenolysis and prevents glycogen buildup2) Increases gluconeogenesis (decrease prdouction of fructose-2,6-bisphosphate decrease phosphofructokinase activity)&lt;br/&gt;3) Increases lipolysis&lt;br/&gt;4) Increases urea production (due to increased gluconeogenesis).</answer>
<resources>BRS2nd: p. 266</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>How could a forensic pathologist determine whether the high concentration in Sunny von Bulow's blood was due to an overdose or her diabetes?</question>
<answer>Proinsulin is synthesized as a single chain peptide. Proteases break down the proinsulin into insulin and a C peptide, both of which are secreted into the blood. The insulin which diabetics self-adminster though does not have the C peptide. Thus if von Bulow's blood has a correspondingly high C peptide concentration, it was her diabetes.</answer>
<resources>BRS2nd: p. 266</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>Insulin is called the anabolic hormone because it promotes all of the following EXCEPT</question>
<multiple_choice>
<choice>The net synthesis of protein from amino acids</choice>
<choice>The storage of glucose as glycogen</choice>
<choice>The conversion of amino acids to glucose</choice>
<choice>The conversion of glucose to fatty acids and triacylglycerol</choice>
<choice>The storage of dietary fats</choice>
</multiple_choice>
<answer>Answer: The conversion of amino acids to glucose. This is a consequence of glucagon</answer>
<resources>http://faculty.une.edu/com/courses/bionut/distbio/obj-512/Chap26-practice%20questions.htm</resources>
<type>exam</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>All of the following statements about hormones and when they exert their major effect are correct EXCEPT</question>
<multiple_choice>
<choice>Glucagon, catecholamines, and cortisol exert a major effect during stress</choice>
<choice>Glucagon, catecholamines, insulin, and cortisol exert a major effect during starvation (prolonged fasting)</choice>
<choice>Insulin exerts a major effect in the fed state</choice>
<choice>Glucagon exerts a major effect in the fasting state</choice>
<choice>Catecholamines exerts a major effect during exercise</choice>
</multiple_choice>
<answer>Glucagon, catecholamines, insulin, and cortisol exert a major effect during starvation (prolonged fasting)</answer>
<resources>http://faculty.une.edu/com/courses/bionut/distbio/obj-512/Chap26-practice%20questions.htm</resources>
<type>exam</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>All of the following actions of glucagon are true EXCEPT</question>
<multiple_choice>
<choice>Glucagon will inhibit glycogen synthesis and activate glycogenolysis</choice>
<choice>Glucagon will inhibit glycolysis in the liver and activate gluconeogenesis in the liver</choice>
<choice>Glucagon will activate fatty acid mobilization (release) in adipose tissue</choice>
<choice>Glucagon will activate triacylglycerol synthesis in liver and adipose</choice>
<choice>Glucagon will remove amino acids for gluconeogenesis and thus increase the mobilization of amino acids from proteins</choice>
</multiple_choice>
<answer>Glucagon will NOT activate triacylglycerol synthesis in liver and adipose.</answer>
<resources>http://faculty.une.edu/com/courses/bionut/distbio/obj-512/Chap26-practice%20questions.htm</resources>
<type>exam</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas" insulin</keywords>
<difficulty>1</difficulty>
<question>What is the machanism for insulin secretion?</question>
<answer>Glucose binds to Glut-2 receptor on pancreatic beta cells. Glucose is oxidized to ATP inside the beta cells which closes K+ channels leading to depoarziation. Depolarization then opens Ca2+ channels leading to an increase in intracelllular Ca2+ and then to secretion of insulin.</answer>
<resources>BRS2nd: p. 266-7</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What effect does insulin have on its own receptors in target tissues?</question>
<answer>Insulin down-regulates its own recepters on target tissues. Therefore the number of recepters is increased in starvation and decreased in obesity (is that why the obese become insulin resistant??).</answer>
<resources>BRS2nd: p. 267</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>How does insulin decrease blood glucose concentration?</question>
<answer>1) Increases uptake of glucose in target cells&lt;br/&gt;2) Promotes formation of glycogen in muscle and liver and inhibits glycogenolysis.&lt;br/&gt;3) Decreases gluconeogenesis by directing substrate away from glucose formation.</answer>
<resources>BRS2nd: p. 267</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What effect does insulin have on blood fatty acid and ketacid concentrations?</question>
<answer>In adipose tissue, insluin stimulates fat deposition and inhibits lipolysis. The subsequence decrease in acetyl CoA prevents the liver from forming ketoacids.</answer>
<resources>BRS2nd: p. 267</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>T/F: Insulin is anabolic.</question>
<answer>True: Insulin stimulates amino acid uptake into cells, increases protein synthesis and inhibits protein degradation.</answer>
<resources>BRS2nd: p. 267</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What effect does insulin have blood K+ levels?</question>
<answer>Insulin increases K+ uptake into cell and thus decreases the K+ concentration in blood.</answer>
<resources>BRS2nd: p. 267</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>A woman is brought to the ER. She is hypotensive and breathing rapidly; her breath has the odor of ketones. Analysis of her blood shows severe hyperglycemia, hyperkalemia, and blood gas values that are consistent with metabolic acidosis. What is causing her condition?</question>
<answer>1) Hyperglycemia: results from insulin deficiency.&lt;br/&gt;2) Hypotension: results from ECF volume contraction due to inability to reabsorb excess glucose.&lt;br/&gt;3) Metabolic acidosis: caused by overproduction of ketoacids from lipolysis triggered by high levels of glucagon&lt;br/&gt;4) Hyperkalemia: insulin triggers K+ uptake into cells; no insulin, reduced updtake.</answer>
<resources>BRS2nd: p. 268</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What cells of the pancreas secrete somatostatin? What effects does somatostatin have?</question>
<answer>Somatostatin is secreted by delta cells of the pancreas. It inhibits the secretion of insulin, glucagon and gastrin.</answer>
<resources>BRS2nd: p. 268</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What controls secretion of PTH?</question>
<answer>1) Decreased serum Ca2+ concentration leads to aincrease in PTH secretion by parathyroid chief cells. &lt;br/&gt; 2) Mild decreases in serum Mg2= stimulate PTH secretion but severe decreases in Mg2+ inhibit PTH secretion.</answer>
<resources>BRS2nd: p. 270</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What are the actions of PTH?</question>
<answer>1) Increased bone resorption: causes increase in blood Ca2+ and phosphate.&lt;br/&gt;2) Inhibits renal phosphate reabsorption in proximail tubule, increasing phosphate excretion.&lt;br/&gt;3) Increases renal Ca2+ reabsorption in distal tubule.&lt;br/&gt;4) Increaes intestintal Ca2+ absorption by stibuluate prodyction of 1,25-hyhydroxycholcalciferol in kidney.</answer>
<resources>BRS2nd: p. 270</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>Primary hyperparathyroidism is commonly caused by parathryoid adenoma. All of the following are true EXCEPT</question>
<multiple_choice>
<choice>Increase in serum [Ca2+]</choice>
<choice>Decrease in serum [phosphate]</choice>
<choice>Increase in urniary phosphate excretion</choice>
<choice>Increase in urinary Ca2+ excretion</choice>
<choice>Decrease in bone resorption</choice>
</multiple_choice>
<answer>Primary hyperparathyroidism causes an INCREASE in bone resorption.</answer>
<resources>BRS2nd: p. 270-1</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>Hypoparathyroidism is most commonly a result of thyroid surgery or is congential. Of the following, determine if each statement is true or false:</question>
<multiple_choice>
<choice>Serum [Ca2+] decreases</choice>
<choice>Serum [phosphate] increases</choice>
<choice>Urinary phosphate exrcetion decreases</choice>
</multiple_choice>
<answer>All are true.</answer>
<resources>BRS2nd: p. 271</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"endocrine pancreas"</keywords>
<difficulty>1</difficulty>
<question>What are the causes of renal osteodystrophy?</question>
<answer>Chronic renal failure leads to a decreased GFR and decreased filtration of phosphate and increased serum [phosphate]. Increased phosphate complexes with Ca2+ reducing free Ca2+ and stimulating PTH secretion (secondary hyperparathyroidism). Diseased renal tissue also leads to decreased production of 1,25-dihydroxycholecalicferol. This and the increased PTH lead to renal osteodystrophy in which there's increased bone sesorption and ostemalacia.</answer>
<resources>BRS2nd: p. 272</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"male reproduction"</keywords>
<difficulty>1</difficulty>
<question>What is the active form of testosterone and where is it activated?</question>
<answer>Testosterone is activated in accessory sex organs which contain 5alpha-reductase. This enzymes converts testosterone to dihydrotestosterone, the active form.</answer>
<resources>BRS2nd: p. 275</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"male reproduction"</keywords>
<difficulty>1</difficulty>
<question>Describe the up-regulatory pathway of testosterone beginning with the role of the hypothalamus and ending with the effects on the individual cells of the testes.</question>
<answer>1) The arcuate nuclei of the hypothalamus release GnRH which in turn stimulates the anterior pitutitary to secrete FSH and LH.&lt;br/&gt;2) FSH acts on Sertoli cells to maintain spermatogenesis.&lt;br/&gt;3) LH acts on Leydig cells to promote testerone synthesis.</answer>
<resources>BRS2nd: p. 275</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"male reproduction"</keywords>
<difficulty>1</difficulty>
<question>Describe the pathway through which testosterone is downregulated.</question>
<answer>Testosterone inhibits release of GnRH from the hypothalamus and LH from the anterior pituitary.</answer>
<resources>BRS2nd: p. 275</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"male reproduction"</keywords>
<difficulty>1</difficulty>
<question>The Sertolic cells of the testes secrete inhibin. What does it do?</question>
<answer>Inhibin inhibits the secretion of FSH by the anterior pituitary.</answer>
<resources>BRS2nd: p. 275</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"male reproduction"</keywords>
<difficulty>1</difficulty>
<question>Describe the actions of testosterone and dihydrotestosterone.</question>
<answer>1) Prenatal differentiation of the Wolffian ducts (testosterone) and external gentitalia (DHT).&lt;br/&gt;2) Development of secondary sex characteristics at puberty.&lt;br/&gt;3) Pubertal growth spurt (testosterone).&lt;br/&gt;4) Maintains spermatogenesis in Sertoli cells (paracrine effect of testosterone).&lt;br/&gt;5) Increaes seize and secretory activty of accessory sex organs (DHT).&lt;br/&gt;6) Increases libido (testosterone).</answer>
<resources>BRS2nd: p. 276</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"male reproduction"</keywords>
<difficulty>1</difficulty>
<question>Determine whether each of the following are T/F:</question>
<multiple_choice>
<choice>In childhood, hormone levels are lowest and LH > FSH.</choice>
<choice>At puberty and during reproductive years, hormone levels increase and LH > FSH.</choice>
<choice>In senescence, hormone levels are lowest and FSH > LH.</choice>
</multiple_choice>
<answer>(False) In childhood, hormones levels are lowest BUT FSH is greater than LH.&lt;br/&gt;(True) At puberty and during reproductive years, hormone levels increase and LH>FSH.&lt;br/&gt;(False) In senescence, hormone levles are HIGHEST and FSH>LH.</answer>
<resources>BRS2nd: p. 276</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>What is the precursor of estrogen? Where and how is this precursor converted to estrogen?</question>
<answer>Theca cells produce testerone (stimulated by LH) and diffuses into nearby granulosa cells. Here, aromatase convertes testerone to 17B-estradiol (stimulated by FSH).</answer>
<resources>BRS2nd: p. 276</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>What are the four major effects of FSH and LH in females?</question>
<answer>1) Steroidogenesis in the ovarian follicle and corpus luteum.&lt;br/&gt;2) Follicular development beyond the antral stage.&lt;br/&gt;3) Ovulation&lt;br/&gt;4) Luteinization</answer>
<resources>BRS2nd: p. 276</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>What are the primary actions of estrogen?</question>
<answer>1) Has both negative and positive feedback effects on FSH and LH secretion.&lt;br/&gt;2) Causes maturation and maintenance of female accesory sex organs.&lt;br/&gt;3) Causes development of female secondary sex characteristics at puberty.&lt;br/&gt;4) Causes development of breasts.&lt;br/&gt;5) Up-regulates estrogen, LH, and progesterone recepters.&lt;br/&gt;6) Causes proliferation and development of ovarian granulosa cells.&lt;br/&gt;7) Maintains pregnancy&lt;br/&gt;8) Lowers uterine threshold to contractile stimuli during prenancy.&lt;br/&gt;9) Stimulates prolactin secretion (but then blocks its action on the breast).</answer>
<resources>BRS2nd: p. 278</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>What are the primary actions of progesterone?</question>
<answer>1) Has negative feedback effects on FSH and LH secretion during luteal phase.&lt;br/&gt;2) Maintains secretory activity of the uterus during the luteal phase.&lt;br/&gt;3) Maintains pregnancy&lt;br/&gt;4) Raises the uterine threshold to contractile stimuli durin pregnancy.&lt;br/&gt;5) Participates in development of breasts.</answer>
<resources>BRS2nd: p. 278</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>Describe the follicular phase. Include time length, hormone levels and actions and status of egg.</question>
<answer>1) Days 1-14&lt;br/&gt;2) Primordial follcile develops to graafian stage, atresia of all other follicles.&lt;br/&gt;3) LH and FSH receptors upregulated in theca and granulosa cells.&lt;br/&gt;4) Estradiol levels increase and cause proliferation of uterus.&lt;br/&gt;5) FSH and LH levels are suppressed as estradiol inhibits their release from anterior pituitary.&lt;br/&gt;6) Progesterone levels are low.</answer>
<resources>BRS2nd: p. 278-9</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>Describe ovulation. Include time length and hormone levels and actions.</question>
<answer>1) Occurs 14 days before menses, regardless of cycle length.&lt;br/&gt;2) Burst of estradiol causes secretion of FSH and LH surge.&lt;br/&gt;3) LH surge casues ovluation.&lt;br/&gt;4) Estrogen levels decrease just after ovulation.&lt;br/&gt;5) Cervical mucus increases in quantity; becomes less viscous.</answer>
<resources>BRS2nd: p. 279</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>Describe a luteal phase which does not end in pregnancy. Include time length and hormone levels and actions.</question>
<answer>1) Last 14 days of menstrual cycle.&lt;br/&gt;2) Corpus luteum begins to develop and synthesize estrogen and progesterone.&lt;br/&gt;3) Vascularity and secretory activity of endometrium increase.&lt;br/&gt;4) Basal body temperature increases (progesterone effect on hypothalamic thermoregulatory center).&lt;br/&gt;5) If no fertilization, corpus luteum regresses bt end of phase causing estradiol and progesterone levels to decrease abruptly.</answer>
<resources>BRS2nd: p. 279</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>What prevents the degradation of the corpus luteum when fertilization occurs?</question>
<answer>Human chorionoic gonadotropin (HCG), produced by the placenta,  sustains the corpus luteum.</answer>
<resources>BRS2nd: p. 279</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>What is the corpus luteums primary function?</question>
<answer>To produce estradiol and progesterone which maintain the endometrium, suppress ovarian follicular function (inhibit FSH and LH) and stimulate breast development.</answer>
<resources>BRS2nd: p. 279</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>In the second and third trimesters, what produces progesterone?</question>
<answer>The placenta produces the progesterone.</answer>
<resources>BRS2nd: p. 279</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>In the second and third trimesters, where and how are estrogens produced?</question>
<answer>The fetal adrenal gland syntehsizes dehydroepiandrosterone-sulfate (DHEA-S) which is hydroxylated in the fetal liver. These intermediates go to the placenta where enzymes convert them to estrogens.</answer>
<resources>BRS2nd: p. 280</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>What opposing effects does estrogen have on lactation during pregnancy?</question>
<answer>During pregnancy, estrogen stimulates the anterior pituitary to secrete prolactin. However, lactation does not occur becasue estrogen (and progesterone) block the action of prolactin on the breast.</answer>
<resources>BRS2nd: p. 280</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>How does prolactin act to suppress ovulation?</question>
<answer>1) Inhibits hypothalmic GnRH secretion&lt;br/&gt;2) Inhibits actino f GnRH on anterior pituitary, inhibiting LH and FSH secretion.&lt;br/&gt;3) Opposes action of LH and FSH on ovaries.</answer>
<resources>BRS2nd: p. 281</resources>
<type>review</type>
</q_set>
<q_set>
<subject>physiology</subject>
<section>endocrinology</section>
<keywords>"female reproduction"</keywords>
<difficulty>1</difficulty>
<question>When does menses occur and what causes it?</question>
<answer>Menses occurs during days 1-4 of the menstrual cycle. It results due to the sudden decrease in estradiol and progesterone.</answer>
<resources>BRS2nd: p. 279</resources>
<type>review</type>
</q_set>
</database>