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<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">Dear Class of 2028,
<o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">I have received questions on the topic of hyperparathyroidism and wanted to provide clarification.
<o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">Hyperparathyroidism is a condition that occurs when the parathyroid glands produce too much parathyroid hormone (PTH).<o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal" style="margin-left:.5in"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">In
<u>primary hyperparathyroidism</u>, there is an intrinsic overactivity of one or more of the parathyroid glands (due to parathyroid adenoma in most cases).
<o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal" style="margin-left:.5in"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">In
<u>secondary hyperparathyroidism</u>, there is a compensatory overactivity of the parathyroid glands in response to a prolonged state of hypocalcemia (due to renal failure or inadequate nutrition).
<o:p></o:p></span></p>
<p class="MsoNormal" style="margin-left:1.0in"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">With
<b><u>secondary hyperparathyroidism</u></b>, one could be referring to <b>renal secondary hyperparathyroidism</b> OR one could be referring to
<b>nutritional or malabsorption secondary hyperparathyroidism</b>. <i>Renal </i>secondary hyperparathyroidism and
<i>nutritional</i> hyperparathyroidism are both conditions characterized by elevated PTH levels, but they arise from different underlying causes.
<i>Renal</i> secondary hyperparathyroidism is primarily linked to kidney disease, while
<i>nutritional </i>secondary hyperparathyroidism stems from nutrient/dietary deficiencies. In nutritional secondary hyperparathyroidism, decreased dietary intake or malabsorption results in low vitamin D (thus
</span><span style="font-size:10.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">generally</span><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"> low calcium and low phosphate). People with kidney disease
(and thus potentially renal secondary hyperparathyroidism) will have high phosphate because the diseased kidney is unable to excrete phosphate like it normally does. Please see slide 42 of MSK 05.<o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><img width="987" height="368" style="width:10.2812in;height:3.8333in" id="Picture_x0020_3" src="cid:image002.jpg@01DB62A5.CF8000C0"></span><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">Please feel free to talk to myself, Dr. Alekseev, or Dr. Fink (MSK Course Director) if this remains unclear.</span><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"> <o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">We can also talk after my lecture on Tuesday.
<o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">Know that hyperparathyroidism will be covered again in later system courses (e.g. Renal System, Endocrine System).</span><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif"><o:p> </o:p></span></p>
<p class="MsoNormal"><span style="font-size:12.0pt;font-family:"Bahnschrift Light SemiCondensed",sans-serif">All the best,
<o:p></o:p></span></p>
<p class="MsoNormal"><o:p> </o:p></p>
<p class="MsoNormal"><span style="font-size:11.5pt;font-family:"Arial Narrow",sans-serif;color:#404040">Bonnie Brenseke, DVM, PhD, DACVP<br>
Associate Professor and Biomedical Chair of Pathology <o:p></o:p></span></p>
<p class="MsoNormal"><span style="font-size:11.5pt;font-family:"Arial Narrow",sans-serif;color:#404040">School of Osteopathic Medicine | Campbell University<br>
Levine Hall Office #165 | (910) 893-1746<o:p></o:p></span></p>
<p class="MsoNormal"><a href="http://medicine.campbell.edu/"><span style="color:windowtext;text-decoration:none"><img border="0" width="309" height="38" style="width:3.2187in;height:.3958in" id="Picture_x0020_1" src="cid:image004.png@01DB62A5.CF8000C0" alt="cid:image001.png@01D2F654.FC2B2F20"></span></a><o:p></o:p></p>
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