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Bupron SR

By N. Eusebio. McDaniel College.

The neurologic examination showed severe muscle weakness buy generic bupron sr 150mg online, especially in the proximal arms and legs discount 150mg bupron sr otc, where the mus- cles seemed atrophied 150mg bupron sr with mastercard. Sam Atotrope discount 150 mg bupron sr with amex, a 42-year-old jeweler order bupron sr 150mg visa, noted increasingly severe headaches behind his eyes sometimes associated with a “flash of light” in his visual fields. At times his vision seemed blurred, making it difficult to perform some of the intricate work required of a jeweler. He consulted his ophthalmologist, who was impressed with the striking change in Sam’s facial features that had occurred since he last saw the patient 5 years earlier. The normal skin creases in Sam’s face had grown much deeper, his skin appeared to be thickened, his nose and lips appeared more bulbous, and his jaw seemed more prominent. The doctor also noted that Sam’s hands appeared bulky, and his voice had deepened. An eye exam- ination showed that Sam’s optic nerves appeared slightly atrophied, and there was a loss of the upper outer quadrants of his visual fields. PHYSIOLOGIC EFFECTS OF INSULIN The effects of insulin on fuel metabolism and substrate flux were considered in many of the earlier chapters of this book, particularly in Chapter 26. Insulin stimu- lates the storage of glycogen in liver and muscle and the synthesis of fatty acids and triacylglycerols and their storage in adipose tissue. In addition, insulin stimulates the synthesis in various tissues of more than 50 proteins, some of which contribute to the growth of the organism. In fact, it is difficult to separate the effects of insulin on cell growth from those of a family of proteins known as the somatomedins or the insulin-like growth factors I and II (IGF-I and IGF-II) (see Section III. Finally, insulin has paracrine actions within the pancreatic islet cells. When insulin is released from the cells, it suppresses glucagon release from the cells. PHYSIOLOGIC EFFECTS OF GLUCAGON Glucagon is one of several counterregulatory (contrainsular) hormones. It is syn- thesized as part of a large precursor protein, proglucagon. Proglucagon is produced in the cells of the islets of Langerhans in the pancreas and in the L cells of the intestine. It contains a number of peptides linked in tandem: glicentin-related pep- tide, glucagon, glucagon-related peptide 1 (GLP-1), and glucagon-related peptide 2 (GLP-2). Proteolytic cleavage of proglucagon releases various combinations of its constituent peptides. Glucagon is cleaved from proglucagon in the pancreas and constitutes 30 to 40% of the immunoreactive glucagon in the blood. The remaining immunoreactivity is caused by other cleavage products of proglucagon released from the pancreas and the intestine. Pancreatic glucagon has a plasma half-life of 3 to 6 minutes and is removed mainly by the liver and kidney. Glucagon promotes glycogenolysis, gluconeogenesis, and ketogenesis by stimu- lating the generation of cyclic adenosine monophosphate (cAMP) in target cells. The liver is the major target organ for glucagon, in part because the concentrations of this hormone bathing the liver cells in the portal blood are higher than in the peripheral circulation. Portal vein levels of glucagon may reach concentrations as high as 500 pg/mL. Finally, glucagon stimulates insulin release from the cells of the pancreas. Whether this is a paracrine effect or an endocrine effect has not been established. The pattern of blood flow in the pancreatic islet cells is believed to bathe the cells 786 SECTION EIGHT / TISSUE METABOLISM first and then the -cells. Therefore, the cells may influence -cell function by an endocrine mechanism, whereas the influence of -cell hormone on -cell function is more likely to be paracrine. PHYSIOLOGIC EFFECTS OF OTHER COUNTERREGULATORY HORMONES A.

Digestion Tgb Solemia’s tumor was in the anterior pituitary order 150mg bupron sr fast delivery, by lysosomal with T4 not in an extrapituitary ACTH-producing site buy 150mg bupron sr amex. The protein thyroglobulin (Tgb) is synthesized in thyroid follicular cells and secreted into the colloid generic 150 mg bupron sr with amex. Iodination and coupling of tyrosine residues in Tgb produce T3 and T4 residues 150 mg bupron sr amex, which are released from Tgb by pinocytosis (endocytosis) and lysosomal action purchase bupron sr 150mg online. The coupling of a monoiodotyrosine with a The iodide concentrating or trap- diiodotyrosine (DIT) to form triiodothyronine (T3) is not depicted here. An internal autoregulatory mechanism decreases transport those in the blood, depending on the current of iodide into the cell when the intracellular iodide concentration exceeds a certain size of the total body iodide pool and the threshold and increases transport when intracellular iodide falls below this thresh- present need for new hormone synthesis. The oxidation of intracellular iodide is catalyzed by thyroid peroxidase (located at In areas of the world in which the the apical border of the thyroid acinar cell) in what may be a two-electron oxidation soil is deficient in iodide, hypothy- step forming I (iodinium ion). Iodinium ion may react with a tyrosine residue in the roidism is prevalent. The thyroid protein thyroglobulin to form a tyrosine quinoid and then a 3 -monoiodotyrosine gland enlarges (forms a goiter) in an attempt to produce more thyroid hormone. It has been suggested that a second iodide is added to the ring by sim- United States, table salt (NaCl) enriched with ilar mechanisms to form a 3,5-diiodotyrosine (DIT) residue. Because iodide is added iodide (iodized salt) is used to prevent to these organic compounds, iodination is also referred to as the “organification of hypothyroidism caused by iodine deficiency. T3 and T4 are stored in the thyroid follicle as amino acid residues in thyroglobulin. Under most circumstances, the T4/T3 ratio in The thyroid gland is unique in that it has the capacity to store large thyroglobulin is approximately 13:1. This storage accounts for the low transport proteins in the blood. Of these transport proteins, thyroid-binding globulin overall turnover rate of T3 and T4 in the body. This free fraction of hormone has biologic activity because it is the only form that is capable of diffusing across target cell membranes to interact with intracellular receptors. The transport proteins, therefore, serve as a large reservoir of hormone that can release additional free hormone as the metabolic need arises. The thyroid hormones are degraded in liver, kidney, muscle, and other tissues by deiodination, which produces compounds with no biologic activity. SECRETION OF THYROID HORMONE The release of T3 and T4 from thyroglobulin is controlled by thyroid-stimulating hormone (TSH) from the anterior pituitary. TSH stimulates the endocytosis of thy- roglobulin to form endocytic vesicles within the thyroid acinar cells (see Fig. Lysosomes fuse with these vesicles, and lysosomal proteases hydrolyze thyroglobulin, releasing free T4 and T3 into the blood in a 10:1 ratio. In various tis- sues, T4 is deiodinated, forming T3, which is the active form of the hormone. TSH is synthesized in the thyrotropic cells of the anterior pituitary. Its secretion Hypothalamus is primarily regulated by a balance between the stimulatory action of hypothalamic thyroid-releasing hormone (TRH) and the inhibitory (negative feedback) influence TRH of thyroid hormone (primarily T3) at levels above a critical threshold in the blood – bathing the pituitary thyrotrophs. TSH secretion occurs in a circadian pattern, a surge beginning late in the afternoon and peaking before the onset of sleep. In addition, + TSH is secreted in a pulsatile fashion with intervals of 2 to 6 hours between peaks. TSH stimulates all phases of thyroid hormone synthesis by the thyroid gland, Pituitary including iodide trapping from the plasma, organification of iodide, coupling of monoiodotyrosine and diiodotyrosine, endocytosis of thyroglobulin, and proteoly- sis of thyroglobulin to release triiodothyronine (T3) and tetraiodothyronine (T4) (see TSH Fig. In addition, the vascularity of the thyroid gland increases as TSH stim- – ulates hypertrophy and hyperplasia of the thyroid acinar cells. The predominant mechanism of action of TSH is mediated by binding of TSH to its specific receptor on the plasma membrane of the thyroid acinar cell, leading to an increase in the concentration of cytosolic cAMP. Recent evidence indicates, T3 however, that TSH also increases the cellular levels of inositol trisphosphate and T3 2 T4 + diacylglycerol, causing a rise in cytosolic Ca within the thyroid cell.

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