Guyton and Hall Physiology Chapter 80 - Parathyroid Hormone

How does an increase in extracellular fluid calcium concentration impact the nervous system?

What is the primary mechanism by which bones act as calcium reservoirs?

What is the effect of increased calcium ion concentration on the heart's QT interval and gastrointestinal tract activity?

How does the pH of extracellular fluid affect the relative concentrations of $HPO_4^=$ and $H_2PO_4^-$?

At what concentration of blood calcium do depressive effects on the nervous system typically start to manifest?

What is the consequence of extreme hypocalcemia in laboratory animals that is rarely observed in human patients?

How does vitamin D primarily facilitate calcium absorption in the intestines?

What characterizes the importance of TNAP in bone mineralization?

What is the pivotal role of osteoprotegerin (OPG) in bone remodeling?

How does continual bone remodeling contribute to bone health?

What mechanism underlies bone remodeling in response to increased mechanical stress?

How does the body maintain a stable plasma concentration of 25-hydroxycholecalciferol?

Which primary factor stimulates the conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol within the kidneys?

How does 1,25-dihydroxycholecalciferol regulate plasma calcium concentration?

What is the primary effect of 1,25-Dihydroxycholecalciferol on intestinal calcium absorption?

In the absence of vitamin D, what is the effect on PTH's ability to cause bone resorption?

How does PTH influence phosphate handling in the kidneys?

How does PTH regulate blood calcium levels?

Chief cells in the parathyroid glands primarily synthesize what?

What mediates the primary effects of parathyroid hormone (PTH) on its target organs??

What is the correlation between the calcium ion concentration in extracellular fluid and parathyroid hormone (PTH) secretion?

What is the rapid phase of calcium phosphate mobilization from bone?

How is calcium transported by the osteocytic membrane system?

Why does increased calcitonin in humans have a limited transient affect?

Which components have notable amount of calcium reserve?

What effect does PTH have on calcium in the urine?

How do radioactive substances impact deposited bone?

What is osteoid, and how does it relate to cartilage during bone formation?

How can bone stress accelerate fracture healing?

Why does increased phosphate levels cause calcium phosphate deposition in the body?

What can vitamin D cause in extreme quantities?

What causes increase in calcitonin secretion?

How can the bone mineral saturation in patients with lower calcium levels remain normal without causing any bone weakness?

Which condition has lower osteoblastic functions with growth and protein anabolism?

What allows for the upper and lower teeth to provide grinding and cutting force between teeth?

What part of the tooth is created from ameloblasts?

What causes the fast recovery of calcium ion concentration after intravenous injection of calcium?

What compensatory mechanism is triggered by even a small decline in extracellular fluid calcium concentration?

What is a significant consequence of extreme hypocalcemia, which is mainly observed in laboratory animals?

How does tissue-nonspecific alkaline phosphatase (TNAP) impact bone calcification?

What is the primary effect of increased PTH secretion on plasma phosphate concentration, and how is this achieved?

Why does the administration or excessive secretion of PTH ultimately lead to evident resorption in all the bones?

What specific action of PTH within the kidneys prevents eventual depletion of calcium from the extracellular fluid and bones?

What best describes the relationship between tensile and compressional strength in bone?

What crucial role do proteoglycans play within the ground substance of bone's organic matrix?

Why are the bones of children less brittle than those of the elderly?

How does mechanical stress from using a bone after a fracture contribute to its healing process?

Following the formation of osteoid, what sequence accurately describes the transformation leading to hydroxyapatite crystals?

After a bone fracture, the healing process leads to the formation of a callus. What is the initial composition of this callus, and how does it evolve?

What mechanism explains why hydroxyapatite crystals typically precipitate only in bone, despite extracellular fluid being supersaturated with calcium and phosphate ions?

Which sequence accurately represents the activation of vitamin D3 in the body to its active form?

What effect does increasing vitamin D intake have on plasma 25-hydroxycholecalciferol concentrations?

What explains the limited lasting impact that increased calcitonin has on plasma calcium concentration in adult humans?

How do the osteoblasts and osteocytes transfer calcium ions from the bone fluid to the extracellular fluid?

How does increased activity of calcium-sensing receptors (CSR) in parathyroid cell membranes affect PTH secretion?

In the context of long-term calcium regulation, how does the body respond when the bone reservoir is either depleted or saturated with calcium?

What role does the osteocytic membrane system play in bone?

Which process describes the initial stage of bone production caused by osteoblasts?

What is particularly unique about osteitis fibrosa cystica regarding PTH?

What substance directly activates preosteoclast cells transforming them into osteoclasts?

What is the mechanism behind increased bone deposition in response to increased physical stress?

In the context of bone remodeling, what describes the activity that promotes bone resorption?

How is vitamin D's effectiveness altered in the absence of the kidneys, and why?

While calcium is being regulated, what is one thing that phosphate does not have during secretion in the kidneys?

What is the main difference between bones of patients with osteoporosis compared with that of osteomalacia?

In hypoparathyroidism, what does the body do with the calcium instead of use?

Extreme quantities of vitamin D can lead to?

What causes the change to the bones during rickets?

During hyperparathyroidism, why do kidney stones arise?

Caries, or teeth erosion, relies on bacteria breaking down?

Caries happens quicker once the enamel?

If broken how does orthodontic intervention push teeth?

Dental enamel contains?

Considering the interplay between calcium absorption, renal excretion, and bone metabolism, what is the most critical reason for maintaining precise control over extracellular fluid calcium concentration?

What is the primary reason most of the ingested calcium is excreted in the feces?

What mechanism explains why the body prioritizes maintaining normal blood calcium levels even when dietary calcium intake is insufficient?

Under what conditions would calcium phosphate crystals most likely begin to precipitate throughout the body?

Why does the body tightly regulate phosphate concentrations if they do not have the same extreme physiological effects as altered calcium levels?

How do osteoblasts affect the osteoclasts?

In addition to its well-known effects on calcium, what is a significant function of Vitamin D regarding phosphate levels?

What role does pyrophosphate play in bone calcification?

What causes a normal person who is vitamin D deficient to get rickets?

After injection of soluble calcium salts, why does the calcium ion concentration normalize quickly?

Which molecule is secreted by the osteoblasts that regulates bone calcification?

In the context of managing bone fractures, what strategies do orthopedic surgeons employ?

Under what circumstances might calcitonin be more effective at reducing hypercalcemia?

Why is maintaining the structural integrity of bone crucial for the skeleton with high loads?

What best encapsulates the role of continual bone remodeling?

How are radioactive substances incorporated into bone, and what are the potential long-term consequences?

How does PTH affect phosphate levels?

What role does the hormone estrogen play in bone remodeling and osteoporosis?

What critical process begins the activation of cholecalciferol?

How does the activation of vitamin D3 differ in hypoparathyroidism?

A patient with limited exposure to the sun starts to develop osteoporosis. How is vitamin D unable to fix that condition on its own?

The osteocytic membrane system's activation enables calcium and phosphate to release, what is happening in the process?

How are the kidneys regulated to ensure the phosphate concentration is controlled?

How does the absence of kidneys alter vitamin D efficacy?

Which is a unique reason primary hyperparathyroidism occur more in women?

What is the underlying principle that best explains why teeth shift during orthodontic treatment?

Which part of enamel makes it more resistance to demineralization by acids?

Following bone reabsorption, what attempts to occur for osteoblastic activity??

What causes rickets to form in adult patients?

Parathyroid hormone (PTH) and calcitonin work independently to regulate calcium and phosphate metabolism.

Extracellular fluid calcium concentration is rigorously maintained and rarely deviates by more than a few percentage points from its normal level.

Increased extracellular calcium concentrations (hypercalcemia) enhance neuronal excitability, potentially leading to seizures.

The majority of the body's phosphate is stored within cells, with bones serving as a minor reservoir.

Approximately 50% of calcium in plasma is bound to proteins, inhibiting its diffusion across capillary membranes.

The ratio of HPO4- to H2PO4- remains constant irrespective of changes in the extracellular fluid's pH.

Chronic hypophosphatemia significantly enhances bone mineralization.

Tetany manifests when blood calcium concentration drops to about 6 mg/dl, representing roughly 35% below normal levels.

Hypocalcemia depresses the nervous system and muscle activity.

An individual typically excretes approximately 90% of their daily calcium intake through urine.

Low calcium concentration promotes increased reabsorption in the late distal tubules and early collecting ducts, minimizing calcium loss in urine.

Cortical bone, comprising approximately 80% of the human skeleton's total bone mass, exhibits higher rates of synthesis and resorption compared to trabecular bone.

Collagen fibers give bone tensile strength, whereas calcium salts provide compressional strength.

Pyrophosphate promotes hydroxyapatite crystal formation in tissues.

The administration of TNAP elevates pyrophosphate levels, inhibiting bone calcification.

The bone contains a type of exchangeable calcium that is always in equilibrium with calcium ions in the intracellular fluids.

PTH stimulates osteoclast activity and bone resorption through a direct mechanism by binding to osteoclast receptors.

Osteoblasts are responsible for bone resorption and degrade bone matrix by secreting proteolytic enzymes and acids.

Estrogen stimulates osteoprotegerin(OPG) production, thereby stimulating bone resorption processes.

Vitamin D directly causes bone calcium absorption.

Match the following forms of calcium with their percentage in the plasma:

Match each condition with its effect on the nervous system:

Match the process with factors stimulating osteoclast activity:

Match the type of bone cell with its primary role in bone metabolism:

Match the component of bone with its primary function:

Match the process with its description:

Match the form of vitamin D with its site of synthesis or activation:

Match each renal transport process with the electrolytes affected by parathyroid hormone:

Match the cause with the disease:

Match the part of the tooth with the description: