Calcium Homeostasis Quiz

Calcium is a vital mineral for numerous bodily functions including bone formation, muscle contraction, and nerve impulse transmission.

The majority of calcium in the body is stored in bones and teeth in an insoluble form.

Parathyroid Hormone (PTH) is a crucial hormone secreted by the parathyroid glands in response to low calcium levels in the blood.

PTH stimulates bone resorption, which is the breakdown of bone tissue to release calcium into the bloodstream.

PTH promotes the reabsorption of calcium in the kidneys, preventing its loss in urine.

PTH indirectly enhances calcium absorption in the intestines by stimulating the production of active vitamin D.

Hypocalcemia is a condition of low calcium levels in the blood, often caused by PTH deficiency or impaired calcium absorption.

Hypercalcemia is a condition of abnormally high calcium levels in the blood, usually due to excessive PTH production or bone disorders.

The active form of vitamin D, 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃), binds to VDRs in the cell nucleus.

The VDR, bound to vitamin D, forms a complex with the retinoid X receptor (RXR) to bind to specific DNA sequences called vitamin D response elements (VDREs) on target genes.

VDR-RXR complex initiates the transcription of vitamin D-responsive genes, leading to increased synthesis of proteins like calcium absorption, bone mineralization, and cell differentiation.

VDRs in the small intestine regulate the synthesis of proteins like TRPV6, calbindin, and PMCA, facilitating active and passive calcium absorption.

VDRs in the kidneys promote calcium reabsorption in the distal convoluted tubules, aiding in maintaining serum calcium levels.

Insufficient VDR activity, either due to vitamin D deficiency or VDR mutations, can lead to bone diseases like rickets or osteomalacia due to poor calcium absorption.

Mutations in the VDR gene can lead to conditions such as Vitamin D-dependent rickets type II (VDDR II), characterized by impaired calcium absorption and bone mineralization.

VDR activity relies on sufficient levels of 1,25(OH)₂D₃, which requires adequate sunlight exposure (UVB) for synthesis.

A hormone produced by the parathyroid glands, responsible for regulating calcium levels in the blood.

PTH secretion is inversely proportional to plasma calcium levels. Low calcium in the blood leads to increased PTH secretion, while high calcium reduces PTH release.

The calcium-sensing receptor (CaR) is a protein that detects calcium levels in the blood. It sits on the surface of cells in the parathyroid glands and kidneys. When blood calcium is high, CaR activates and reduces PTH release.

Vitamin D is a steroid hormone produced in the skin upon exposure to sunlight. It gets activated in the liver and kidneys and then helps the body absorb calcium from food.

The active form of vitamin D, 1,25(OH)2D3, is produced in the kidneys. It promotes calcium absorption in the intestines, bone resorption, and renal reabsorption of calcium.

Calcitonin is a hormone produced by the thyroid gland that helps to decrease blood calcium levels. It mainly works by inhibiting bone resorption, meaning it slows down the breakdown of bones.

Vitamin D receptors (VDRs) are proteins located inside the nuclei of cells in target organs like the intestines, kidneys, and bones. They bind to active vitamin D and then turn on genes that help control calcium absorption and bone metabolism.

The mechanism of calcium regulation involves a complex interplay of hormones like PTH, vitamin D, and calcitonin. These hormones work together to keep blood calcium levels within a narrow range, ensuring proper bone health, muscle function, and nerve transmission.

A G-protein coupled receptor that regulates PTH secretion in response to extracellular calcium levels.

Mutations in the CaR can lead to either hypercalcemia or hypocalcemia, depending on whether the receptor is less or more sensitive to calcium.

Calcimimetics are drugs that activate the CaR, leading to suppressed PTH secretion and lower blood calcium levels. Calcilytics, on the other hand, decrease the sensitivity of the CaR, resulting in increased PTH and higher blood calcium.

Postmenopausal osteoporosis is characterized by increased bone breakdown (osteoclast activity) and reduced bone formation (osteoblast function) due to estrogen deficiency. This leads to weakened bones and a higher risk of fractures.

Treatments for osteoporosis include anti-resorptive agents (bisphosphonates, SERMs) that inhibit bone breakdown and anabolic therapies (teriparatide) that promote bone formation. Calcium and vitamin D supplementation are also crucial for maintaining bone health.

Calcium's movement across cell membranes, usually from areas of high concentration to low, without requiring energy.

The process of reabsorbing calcium back into the bloodstream from the filtered fluid in the kidneys.

The hormone that regulates calcium levels in the blood by increasing its absorption, release from bones, and reabsorption in the kidneys.

A condition where calcium levels in the blood are lower than normal, often leading to muscle spasms and seizures.

A condition where calcium levels in the blood are higher than normal, often causing fatigue, weakness, and kidney stones.

A serious complication caused by high calcium and phosphate levels, leading to calcification and hardening of blood vessels.

The process of degrading bone tissue to release calcium into the bloodstream, stimulated by parathyroid hormone.

The process of incorporating calcium into bone tissue, helping to build and strengthen bones.