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Endocrinology-Ch.4-Bk Notes

by: Michelle Notetaker

Endocrinology-Ch.4-Bk Notes BIOL 4110

Marketplace > University of North Texas > Biology > BIOL 4110 > Endocrinology Ch 4 Bk Notes
Michelle Notetaker
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About this Document

These are more detailed notes from the textbook covering Ch.4.
Dr. Harris D Schwark
Class Notes
Endocrine system
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This 4 page Class Notes was uploaded by Michelle Notetaker on Monday October 3, 2016. The Class Notes belongs to BIOL 4110 at University of North Texas taught by Dr. Harris D Schwark in Fall 2016. Since its upload, it has received 2 views. For similar materials see Endocrinology in Biology at University of North Texas.


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Date Created: 10/03/16
Endocrinology ­ Ch.4 (Textbook notes) Overview: ● Calcium(Ca) & Phosphorous (inorganic phosphate(Pi)):  ­ structure of hard tissues (bones & teeth) and metabolic regulation/signaling  pathways. ● 2 primary sources of Ca & Pi:  ­ Diet and Skeleton. ● Calcitonin, Calcitriol (1,25­dihydroxyvitamin D) & Parathyroid hormone (PTH)  regulate intestinal absorption and release into the blood after bone resorption of Ca & Pi. Ca & Pi plasma concentrations: ● Ca: 50% ionized, 45% protein­bound, 5% complexed. ● Pi: 84% ionized, 10% protein­bound, 6% complexed. ● Hypocalcemia ­ too little Ca in blood (<8.5mg/dL) ● Hypercalcemia ­ too much Ca in blood (>10.5mg/dL) Regulation of Ca & Pi: Calciotropic hormones: ● PTH ­ Origin ­ Parathyroid glands (principal (chief) cell). ­ Regulated by ­ CaSR (a GPCR) & Calcium­response element. High Ca inhibits  PTH, calcitriol inhibits PTH. ­ Structure ­ secreted as an 84 AA; synthesized as a preproPTH; has < 5 min  half­life. ­ Target/Receptor ­ PTH/PTHrp receptor: PTH1R – high levels in bone  (osteoblasts) and kidney (proximal and distal tubules), PTH2R – high levels in CNS,  pancreas, testis, placenta. ­ Function ­ protects against Hypocalcemia. ● Bone:  osteoblast growth/survival. high levels promotes Ca & Pi release from bone. regulates M­CSF, RANKL, and OPG production by osteoblasts. ● Kidney:  stimulates 1a­hydroxylase activity. stimulates Ca reabsorption by distal nephron (increases Ca ATPase). Inhibits Pi reabsorption by proximal nephron (represses NPT2a). ● 1,25 Dihydroxyvitamin D (Calcitriol) ­ Origin ­ UV light: synthesized by Cholesterol from Vit. D3 & D2. ­ Regulated by ­ magalin: binds to DBP, and by renal 1���­hydroxylase (CYP1���):  stimulated by low serum Ca & inhibited by high serum Ca. ­ Structure ­ circulates blood bound to vitamin D­binding protein (DBP). ­ Target/Receptor ­ Small intestine, Bone, Kidney, Parathyroid gland / nuclear  vitamin D receptor (VDR) that binds to Vit. D­responsive elements. ● Small intestine: Increases Ca absorption ( by increasing TrpV channels, calbindin­D, and PMCA). Marginally increases Pi absorption. ● Bone: Sensitizes osteoblasts to PTH. Regulates osteoid production and calcification. ● Kidney: Minimal actions on Ca reabsorption. Promotes Pi reabsorption by proximal nephron (stimulates NPT2a). ● Parathyroid gland: Directly inhibits PTH gene expression. Directly stimulate CaSR gene expression. Ca & Pi in Bones ● Bone accretion ­ osteoblasts build up bone tissue and bring Ca & Pi into bone. ● Bone resorption ­ osteoclasts break down bone tissue and release Ca & Pi into  blood. ● Osteoblasts ­ Release (M­CSF) monocyte colony­stimulating factor, that acts with RANKL. ­ Derived from osteoprogenitor cells. ­ Contain receptors for PTH and calcitriol. ­ Synthesize organic bone matrix, produce alkaline phosphatase for mineralization. ● Osteocytes ­ Differentiated osteoblasts (trapped in matrix).  ­ Major role in day­to­day calcium regulation.   ● Osteoclasts  ­ Multinucleate, derived from monocytes. ­ Contain calcitonin receptors, but no PTH or calcitriol receptors.  ­ Produce acidic environment to resorb bone matrix. Ca & Pi in the Nephron ● Passive Ca++ reabsorption, through TRP V5 & V6. ● Active Pi reabsorption, through NPT2a, downregulated by PTH. ­ Most filtered Ca is reabsorbed. Hypocalcemic challenge: ­ Low blood Ca (detected by CaSR on parathyroid chief cells) stimulates PTH  secretion. ­ In the kidney, PTH increases Ca levels by increasing fractional resorption of Ca  in renal distal tubules. ­ PTH also inhibits NPT2 activity, which increases Pi excretion. ­ Loss of Pi increases free ionized Ca in the blood. ­ At the bone, PTH stimulates osteoblasts to secrete RANKL, which increases  osteoclast activity. ­ Osteoclast activity increases bone resorption and release of Ca & Pi into blood. Ca++/Pi & immune/inflammatory cells   ● RANK, RANKL, osteoprotegerin are similar to TNFα receptor/NF­κB signaling components.  ­ Activated T cells can express RANKL (stimulated by TNF­α, interleukins…  ● Inflammatory bone disease is associated with increased RANKL­toosteoprotegerin ratios ­ Leads to bone erosion and osteoporosis. Regulation of Ca++/Pi metabolism by gonadal and adrenal steroid hormones  ● Estadiol  ­ Stimulates Ca++ absorption in intestine, reabsorption in kidney. ­ Promotes osteoblast survival and osteoclast apoptosis.  ● Glucocorticoids have opposite effects. Disorders of Ca & Pi regulation Hyperparathyroidism  • Kidney stones  • Osteoporosis  • GI disturbances, peptic ulcers, nausea, constipation  • Muscle weakness, decreased muscle tone  • Depression, lethargy, fatigue, mental confusion  • Polyuria  • Low serum phosphate, high serum calcium Hypoparathyroidism  • Tetany, convulsions, paresthesias, muscle cramps  • Decreased myocardial contractility  • First­degree heart block  • CNS problems, including irritability and psychosis  • Intestinal malabsorption  • Low serum calcium, high serum phosphate concentration  Vitamin D deficiency  ­ Results in hypocalcemia, hypomagnesemia, decreased GI absorption of Ca++  and Pi. ­ These changes cause increased PTH, increased bone resorption.  ● Rickets: vitamin D deficiency before skeletal maturation.  ● Osteomalacia: inadequate bone mineralization after skeletal growth is complete.


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