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CHAPTER 1

  • 1–1. (b) Hormones bind to specific receptors in their target cells. Lipid-soluble hormones bind to intracellular receptors. Hormone binding to binding proteins increase their half-life. Peptide hormones bind to cell membrane receptors. Thyroid hormones are the only nonsteroid hormones that bind to intracellular receptors. They are transported into the cell.

  • 1–2. (e) Changes in mineral and nutrient plasma levels (eg, calcium or glucose) affect hormone release. Pituitary tumors can result in either deficient or excessive hormone production. Transatlantic flight can disrupt circadian rhythms affecting hormone release. Strenuous exercise (as in training for the Olympics) is associated with decreased gonadotropin-releasing hormone (GnRH) release.

  • 1–3. (d) Hormones may inhibit their release through an autocrine mechanism. The substrate a hormone regulates (eg, calcium or glucose) directly regulates release of insulin and parathyroid hormone. Negative feedback regulation can occur at the level of the organ releasing the hormone, at the pituitary or in the hypothalamus. Feedback inhibition may be exerted by nutrients (calcium) and hormones (cortisol).

  • 1–4. (c) The structure of the hormone dictates location of its receptor. This large glycosylated peptide cannot cross the plasma membrane, so it will bind to a cell membrane receptor. It will likely undergo degradation, so it will not be excreted intact in the urine. Hormones do not directly bind to adenylate cyclase. They bind to receptors that couple with diverse signaling mechanisms.

  • 1–5. (d) The response to a hormone binding to a G protein–coupled receptor is dictated by the alpha subunit. Hormone binding to a receptor coupled to a Gαs will result in activation of adenylate cyclase and increased cAMP. Binding to a Gαq would result in stimulation of phospholipase C. Hormone binding to GPCR does not produce activation of tyrosine kinase. Binding to ligand-gated channels produces changes in Na flux.

CHAPTER 2

  • 2–1. (b) Urinary output is 10 times higher than normal (1.5 L/d). This patient suffered traumatic brain injury that disrupted his hypothalamic-neurohypophyseal axis. The large urine volume is the result of decreased arginine vasopressin (AVP) release and decreased water reabsorption (neurogenic diabetes insipidus). Serum sodium and osmolarity will be high because of the excess in water losses.

  • 2–2. (b) The high volume of diluted urine (low sodium and low osmolality) match the description of the patient’s clinical presentation.

  • 2–3. (c) This patient’s problem is most likely associated with decreased freewater reabsorption because of lack of arginine vasopressin (AVP)–stimulating aquaporin 2 insertion into the luminal membrane of the collecting duct. Low AVP levels reflect low production and release of AVP. Without adequate AVP-mediated receptor stimulation, there is no reason to expect increased urinary release of cyclic 3′,5′-adenosine monophosphate (cAMP). Nothing suggests that there is increased sodium reabsorption in this individual.

  • 2–4. (c) Throughout pregnancy, uterine changes will make the tissue more responsive to oxytocin-receptor stimulation. This is the result of increased prostaglandin synthesis, decreased β-adrenergic receptor expression, increased gap junction formation, and increased oxytocin receptor expression. These ...

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