EM1607B "Cardiovascular Consequences of Parathyroid Dysfunction: Implications of Management for PTH Excess, Insufficiency, and Resistance" (IM GR-070816)
The purpose of the presentation is to highlight known and novel interactions between the prototypic osteotropic hormone, parathyroid hormone, and cardiovascular disease. Preclinical genetic models, patient-oriented investigation, and epidemiology converge to indicate that there is a normal “set point” for parathyroid hormone receptor signaling with respect to cardiovascular physiology – and that PTH excess, insufficiency, or acquired resistance arising in the setting of metabolic disorders negatively impacts cardiovascular health. While some of the negative consequences can be attributed to globally altered calcium and phosphate homeostasis, powerful data emerging from preclinical models demonstrate that the cardiovascular system is a direct target for regulation by PTH and the PTH-related polypeptide, PTHrP.
UT Southwestern faculty, fellows, residents and medical students, community physicians, nurse clinicians, physician assistants and nurses.
At the conclusion of this activity, the participant should be able to:
- Describe the actions of parathyroid hormone (PTH) on cardiovascular physiology as directly conveyed by vascular signaling vs. indirect actions via the global regulation of calcium and phosphate homeostasis.
- Explain how chronic elevations in endocrine PTH production perturb paracrine signals dependent upon PTH related polypeptide (PTHrP) - regulation of their shared PTH/PTHrP receptor.
- Anticipate the untoward cardiovascular consequences of excessive or insufficient PTH levels in patients as influenced by the presence or absence of intact renal function.
Dwight Towler, M.D., Ph.D.
J.D. and Maggie E. Wilson Distinguished Chair in Biomedical Research
Division of Endocrinology
- 1.00 AMA
Activities should be run with recent versions of common browsers, including Internet Explorer, Firefox and Google Chrome