Exam #4: Calcium and Bone Physiology Flashcards

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1
Q

List the plasma forms of calcium.

A

There are three forms of Ca++ in the plasma:

1) Free/ ionized Ca++ (50%)
2) Calcium that is bound to protein i.e. albumin (40%)
3) Ca++ bound to small diffusible anions (10%)

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2
Q

In which form is ~ 50% of the total calcium?

A

Free/ ionized Ca++

*Note that this is the only form of Ca++ that is biologically active & regulated

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3
Q

Which forms of Ca++ are filtered in the glomerulus?

A

Ca++ that is NOT protein bound i.e. 60% of the total Ca++ in plasma is filtered at the glomerulus

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4
Q

How does pH effect Ca++ in the plasma?

A

Alkaline pH= more Ca++ bound to protein

Acidic pH= less Ca++ bound to protein

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5
Q

What are the symptoms of hypocalcemia?

A

Hypocalcemia causes threshold to become CLOSER to membrane potential (more negative), which makes nerves & muscles MORE excitable. Symptoms include:

1) Hypocalcemic tetany
2) Latent tetany revealed by Trousseau or Chvostek sign
3) Paresthesias
4) Laryngospasm
5) Seizures
6) Syncope, CHF, and angina

*Chovstek sign= tapping on the facial nerve that elicits twitching of the facial muscles
Trousseau sign= carpopedal spasm upon inflation of a blood pressure cuff

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6
Q

What are the symptoms of hypercalcemia?

A

Hypercalcemia causes threshold to more FARTHER from resting membrane potential (more positive), making nerves and muscles LESS excitable. Symptoms include:

1) Fatigue
2) Muscle weakness
3) Constipation
4) Polyuria
5) Kidney stones
6) Coma
7) Cardiac arrest

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7
Q

Describe the regulation of plasma Ca++.

A
  • Ca++ homeostasis involves the coordinated interaction of the: bone, kidneys, and GI tract
  • Balance is attained when renal excretion= GI absorption of Ca++

On a daily basis:

  • 1,000mg Ca++ ingested but only 350mg absorbed in the GI tract
  • 150 mg secreted into the salivary, pancreatic, and intestinal fluids
  • Net 200mg is absorbed, which much be excreted by the kidneys to be in balance

*Note that 1,25-dihydroxycholecaliferol (active Vitamin D) increases GI absorption of Ca++

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8
Q

What hormone increased GI absorption of Ca++?

A

Active form of Vitamin D

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9
Q

Describe the regulation of plasma phosphorus.

A

GI Tract: most of the dietary phosphorus is absorbed
- Vitamin D controls uptake

Bone: phosphorus is part of the major bone crystalline salt, hydroxapatite

Kidney: at low levels all phosphate is reabsorbed but at higher & higher levels some is excreted

  • PTH increases phosphate excretion
  • Fibroblast growth factor 23 (FGF 23) is a peptide hormone synthesized by osteoblasts and osteocytes that increases renal excretion of phosphate
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10
Q

Why does hydroxyapatite precipitate in bone and not in other tissues?

A

Inhibitors found in other body tissues including plasma prevent precipitation

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11
Q

Outline the mechanism of bone growth and calcification.

A

1) Osteoblasts secrete collagen and ground substance
2) Osteoblasts become trapped in osteoid and become osteocytes
3) Ca++ salts precipitate onto collagen and then hydroxyapatite crystals form

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12
Q

What cells are responsible for bone deposition?

A

Osteoblasts

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13
Q

Which cell type is responsible for bone resorption?

A

Osteoclasts

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14
Q

Describe bone remodeling.

A

Bone remodeling, or the deposition of new bone and reabsorption of old bone, is a continuous process

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15
Q

What is the general function of PTH in bone remodeling?

A

Stimulation of osteoclasts and bone resorption

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16
Q

How does PTH stimulate bone resorption?

A

PTH stimulates bone resorption indirectly:

1) Binds osteoBLASTS and causes them to release cytokines 2) Cytokines, osteoprotegerin ligand (OPLG) activate receptors on preosteoCLAST cells
3) PreosteoCLAST cells differentiate into osteoCLASTS that promote bone resorption

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17
Q

What are the roles and alternate names of: OPGL and OPG? Which increases bone resorption?

A

OPLG= “Osteoprotegerin Ligand” is a cytokine released from osteoBLASTS that induces the differentiation of osteoCLASTS in response to PTH binding to PTH receptors on osteoBLASTS

  • OPLG thus increases bone resorption
  • OPLG is also called “RANK Ligand”

OPG= “Osteoprotegerin,” is a cytokine produced by osteoBLASTS that INHIBITS bone resorption by acting as a decoy receptor for OPGL

18
Q

What is the name for this most active form of vitamin D?

A

1,25-dihydroxycholecalciferol

19
Q

Where is vitamin D3 converted (2 steps, 2 organs) into the most active form of vitamin D?

A

Liver= cholecalciferol–>25-hydroxycholecalciferol

Kidney= PTH converts 25-hydroxycholcalciferol into 1,25-dihydroxycholecalciferol
- Enzyme= 1-alpha hydroxylase & is essential for the formation of ACTIVE Vitamin D

20
Q

What hormone is required for the kidneys to convert Vitamin D into its active form?

A

PTH

21
Q

What is the function of Vitamin D in the GI tract?

A

Stimulation of Ca++ & phosphate absorption

22
Q

What is the function of Vitamin D in the Kidney?

A

Stimulation of Ca++ & phosphate reabsorption

23
Q

What is the function of Vitamin D on the bones?

A

Promotes PTH activity on osteoclasts i.e. promotes PTH mediated bone resorption

24
Q

What is the dose-dependent effect of Vitamin D on the bones?

A

Small amounts of Vitamin D promote calcification

25
Q

What is osteomalacia?

A

Softening of new bone in adulthood due to deficient mineralization–>bending in weight-bearing bones
- Caused by a failure of a damaged kidney to produce the active form of Vitamin D

26
Q

Describe how/why renal disease can cause osteomalacia.

A
  • Kidney is required for the formation of the active form of Vitamin D
  • Vitamin D promotes bone calcification
  • Without Vitamin D, bones are soft due to deficient calcification/ mineralization
27
Q

What is the primary stimulus for PTH secretion?

A

Low ECF Ca++

28
Q

What is the general function of PTH?

A

PTH generally functions to regulate the concentration of Ca++ in the ECF; it increases Ca++ in the ECF BUT DECREASE phosphate

*****Note that a lack of PTH will lead to death from hypocalcemia tetany

29
Q

Why is the action of PTH to decrease phosphate important?

A

Increase in Ca++ & decrease in phosphate prevents crystallization of calcium phosphate

30
Q

What are the actions of PTH on the kidney?

A

1) PTH increases the amount of Ca++ reabsorbed in the distal portions of the nephron
2) PTH inhibits phosphate reabsorption from the kidney
3) PTH increases 1a hydroxylase, the enzyme in the kidney that forms active Vitamin D

31
Q

What is the action of PTH in regards to Vitamin D?

A

1) Increases the enzyme that forms active Vitamin D in the kidney
2) By the action of Vitamin D (indirect), increases uptake of Ca++ & phosphorus from the GI

32
Q

What is the function of Calcitonin (CT)?

A

Decrease bone resorption & Ca++ release

33
Q

What is the stimulus for CT release?

A

Elevated plasma Ca++

34
Q

What are the causes and symptoms of primary hyperparathyroidism?

A

Primary hyperparathyroidism is caused by enlargement of one or more of the parathryoid glands, leading to hypercalcemia and hypophosphatemia. Symptoms include:

  • Ca++ kidney stones
  • Weak bones & bone fractures from bone resorption
  • Constipation & excessive urination
35
Q

What are the causes and symptoms of secondary hyperparathyroidism?

A
  • Secondary hyperparathyroidism occurs in patients with diseases that cause chronically low plasma Ca++
  • Low ECF Ca++ leads to COMPENSATORY hyperstimulation of the parathyroid gland, hypertrophy, & HYPERPARATHYROIDISM
  • Symptoms are the same as for primary hyperparathyroidism
36
Q

What are the causes and symptoms of hypoparathyroidism?

A

Hypoparathyroidism is caused by parathyroidectomy i.e. accidental damage during thyroid surgery, and can lead to a steady decline in plasma Ca++. Symptoms include:

  • Neuromuscular excitability
  • Hypocalcemia tetany
37
Q

What are the causes and symptoms of pseudohypoparathyroidism?

A

Pseudohypoparathryoidism occurs when patients have signs and symptoms of hypoparathyroidism, but PTH levels are normal or elevated. This is caused by a defect in the PTH receptor, or in the tissue response to PTH. Symptoms include symptoms of hypocalcemia.

38
Q

What is the difference in the effects of PTH and FGF23 on PTH and Calcitriol?

A

BOTH increase phosphate excretion by the kidneys

Opposite effects on calcitriol

  • PTH= increases renal production of calcitriol
  • FGF23= decreases renal production of calcitriol
39
Q

What is the role of estrogen in bone remodeling?

A

Estrogen stimulates OPG production, which is a cytokine that acts as a decoy for OPGL

**Thus, estrogen PREVENTS bone resorption, which is why post-menopausal women are at increased risk for osteoporosis

40
Q

What is the effect of glucocorticoids & PTH on OPG?

A

Decreased synthesis of OPG i.e. bone resorption