4300 Unit 3

• Where are iCa and Pi found in bone? iCa and Pi are present in bone as hydroxyapatite crystals.
• How is iCa distributed in extracellular fluid (ECF)? In ECF, iCa is mostly ionized or bound to proteins.
• What hormonal effects increase iCa and Pi levels? Parathyroid hormone (PTH) and calcitriol stimulate release from bones, GI absorption, and renal reabsorption.
• How do Calcitonin and FGF23 affect iCa and Pi levels? Calcitonin and FGF23 decrease iCa and Pi levels by inhibiting their release from bones and renal reabsorption.
• How do Parathyroid Hormone (PTH) and Calcitriol increase ionized calcium (iCa) and phosphate (Pi) levels in the blood? By stimulating the release of iCa and Pi from bones, enhancing their absorption in the GI tract, and promoting their reabsorption in the kidneys.
• What are the mechanisms through which Calcitonin and FGF23 decrease blood levels of ionized calcium (iCa) and phosphate (Pi)? They inhibit the release of iCa and Pi from bones and prevent their reabsorption in the kidneys.
• What is the role of the vitamin D receptor in regulating calcium levels in the body? The vitamin D receptor, which binds to active Vitamin D, plays a crucial role in regulating calcium levels in the body.
• How are the mechanisms for calcitriol-mediated GI absorption and distal convoluted tubular reabsorption of iCa similar? The mechanisms are similar in how they enhance calcium absorption in the GI tract and promote calcium reabsorption in the distal convoluted tubules of the kidneys.
• What insights can be gained by comparing the action of Parathyroid Hormone (PTH) on renal iCa with calcitriol-mediated mechanisms? Comparing PTH action on renal iCa with calcitriol mechanisms provides insights into how different hormones regulate calcium levels in the body.
• How do calcitriol and PTH differ in their effects on phosphate reabsorption in the proximal nephron? Calcitriol enhances phosphate reabsorption, while PTH inhibits it in the proximal nephron.
• What are the contrasting roles of calcitriol and PTH in bone resorption, and how do calcitonin and FGF23 contribute? Calcitriol enhances bone resorption, PTH stimulates it, while calcitonin and FGF23 inhibit bone resorption.
• Explain the mechanisms of ionized calcium (iCa) and phosphate (Pi) entering the plasma across cell barriers. Ionized calcium (iCa) and phosphate (Pi) cross cell barriers through active transport mechanisms and channels.
• How do PTH, calcitriol, calcitonin, and FGF23 impact the transport mechanisms of ionized calcium and phosphate? PTH and calcitriol enhance ionized calcium and phosphate reabsorption, while calcitonin and FGF23 inhibit it.
• What are the roles of PTH and calcitriol in enhancing ionized calcium and phosphate reabsorption in the kidneys and absorption in the GI tract? PTH and calcitriol promote ionized calcium and phosphate reabsorption in kidneys and absorption in the GI tract.
• What is the role of Klotho in FGF23 functionality? Klotho acts as a co-receptor for FGF23, enhancing its binding to its receptor and regulating phosphate and vitamin D metabolism.
• How does CaSR function in maintaining calcium balance? CaSR detects calcium levels and, when high, inhibits PTH release, lowering blood calcium levels.
• Explain how CaSR works in parathyroid chief cells. Activated CaSR inhibits PTH release from parathyroid chief cells, aiding in decreasing blood calcium levels.
• What is the role of CaSR in renal tubular cells? In renal tubular cells, activated CaSR inhibits calcium reabsorption and promotes calcium excretion, lowering blood calcium levels.
• How do parathyroid hormone (PTH) and low calcium levels influence the conversion of calcifediol to calcitriol? PTH and low calcium levels increase calcitriol activation by stimulating 1-hydroxylase.
• What effect do calcitonin, FGF23, high calcium, or phosphate levels have on calcitriol activation? Calcitonin, FGF23, high calcium, or phosphate levels decrease calcitriol activation by inhibiting 1-hydroxylase.
• How does 24-hydroxylase impact calcitriol levels? Increased 24-hydroxylase activity reduces calcitriol levels, while decreased activity increases calcitriol levels.
• What is the role of hormones like PTH and calcitriol in the regulation of ionized calcium and phosphate levels? PTH and calcitriol promote the release of ionized calcium and phosphate, absorption in the gastrointestinal tract, and reabsorption in the kidneys to raise their blood levels.
• How do calcitonin and FGF23 contribute to reducing ionized calcium and phosphate levels? Calcitonin and FGF23 work to lower ionized calcium and phosphate levels by inhibiting their release from bones and reabsorption in the kidneys.
• How do Parathyroid hormone (PTH) and calcitriol increase levels of ionized calcium and phosphate? By stimulating their release from bones, enhancing absorption in the gastrointestinal tract, and promoting reabsorption in the kidneys.
• What are the roles of Calcitonin and fibroblast growth factor 23 (FGF23) in regulating ionized calcium and phosphate levels? They decrease iCa and Pi levels by inhibiting their release from bones and reabsorption in the kidneys.
• How does the calcium-sensing receptor (CaSR) respond to high calcium levels? CaSR inhibits PTH release and reduces blood calcium levels by inhibiting renal calcium reabsorption.
• What is the effect of CaSR activation in renal tubular cells on blood calcium levels? It promotes calcium excretion, further lowering blood calcium levels.
• Why is understanding the interplay between hormones, CaSR, iCa, and Pi levels crucial? It is essential for comprehending responses to hyperphosphatemia, hypophosphatemia, hypercalcemia, and hypocalcemia.
• What are symptoms of hypocalcemia on the body? Symptoms include muscle cramps, spasms, tingling in hands, feet, lips; in severe cases: seizures, cardiac arrhythmias.
• What are symptoms of hypercalcemia on the body? Symptoms include fatigue, weakness, loss of appetite, nausea, constipation, excessive thirst; in severe cases: kidney stones, bone pain, confusion, dementia.
• How does hypercalcemia affect membrane depolarization? Hypercalcemia decreases excitability of neurons and muscle cells, leading to muscle weakness and fatigue.
• How does hypocalcemia affect membrane depolarization? Hypocalcemia increases excitability, causing muscle spasms, cramps, and tingling sensations.
• What are the effects of hypocalcemia on cardiac myocytes? Hypocalcemia lengthens repolarization phase, leading to prolonged QT interval on EKG, increasing risk of cardiac arrhythmias.
• How are Calcium (iCa) and Phosphate (Pi) distributed in the body? They are present in the bone, Extracellular Fluid (ECF), and Intracellular Fluid (ICF), distributed from the GI tract or by the kidneys and bone.
• What processes are involved in the movement of iCa and Pi in the body? Processes like absorption from the GI tract into the bloodstream, reabsorption, and deposition by the kidneys and bone.
• How do hormones impact the movement of Calcium (iCa) and Phosphate (Pi) in the body? Hormones like PTH, Calcitriol, Calcitonin, and FGF23 act as regulators, influencing the balance of iCa and Pi in the body by managing their transfer.
• How does calcitriol assist in calcium absorption in the body? Calcitriol serves as a 'tour guide,' aiding in iCa absorption in the GI tract and kidneys.
• What different roles do Parathyroid hormone (PTH) and Calcitonin play in calcium regulation? PTH facilitates iCa reabsorption in kidneys, while Calcitonin helps regulate mineral entry into plasma based on body needs.
• Where do PTH, Calcitonin, and FGF23 originate from in the body? Parathyroid hormone (PTH) comes from parathyroid glands, Calcitonin from the thyroid, and FGF23 is produced in the bone.
• How does the calcium-sensing receptor (CaSR) contribute to calcium regulation? CaSR acts as a regulator, signaling the parathyroid gland to adjust PTH production based on iCa levels.