Test 3 - Schricker Flashcards

1
Q

Major causes of Hypercalcemia

A
  1. Primary hyperparathyroidism
  2. Malignant disease
  3. Latrogenic Vitamin D
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2
Q

Major treatments for Hypercalcemia

A

Treatment with bisphosphonates (inhibit osteoclast activity)

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3
Q

What is an indication of hyperparathyroidism?

A

Intact parathyroid hormone

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4
Q

What is the primary cause of hypercalcemia?

A

Parathyroid Hormone-Related Protein

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5
Q

What is PTHrP produced by?

A

Tumors

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6
Q

What are common tumors that produce PTHrP?

A

Breast, Lung, Kidney, Other Solid Tumors

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7
Q

Major causes of Hypocalcemia?

A

Drop in Serum Albumin (adjusted calcium levels)

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8
Q

Major treatments of Hypocalcemia

A

Activate osteoclast activity

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9
Q

T/F: There is an abnormal metabolism of Vitamin D associated with Hypocalcemia?

A

True

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10
Q

Osteoporosis

  1. What is it?
  2. Risk factors?
  3. Treatment
A
  1. Loss of mineral density with age (peak density at 30), increase fractures,
  2. Risk factors: female, smoke, excessive exercise, no exercise, too much caffeine, poor diet
  3. Treatment: estrogen, biphosphates, calcitonin, PTH
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11
Q

Paget’s Disease

  1. Characteristics
  2. Symptoms
  3. Cause
  4. Treatments
A
  1. Large, numerous Osteoclasts. Many Osteoblasts and an increase in alkaline phosphatase.
  2. Symptoms: Large, misshapen bones, less dense/brittle - high serum content of hydroxyproline, pyridinolines, and telopeptides
  3. Cause is unknown. Maybe genetic or early childhood viral infection.
  4. Treatments: Bisphosphonates and calcitonin
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12
Q

Osteomalacis

  1. What does it cause?
  2. Associated issue
A
  1. Defects in Hydroxyapatite formation due to vitamin D deficiency
  2. Rickets
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13
Q

What is Rickets?

A

Bone and Muscle weakness/skeletal deformity. Due to inhibited Vitamin D metabolism

Noticed during the industrial revolution - lack of sunlight due to pollution and narrow alleys

Treatment - Cod Liver Oil

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14
Q

What will you notice on teeth because of Rickets?

A

The dentin will have “gaps” since it does not remodel like bone

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15
Q

What is the mineral component of bone?

A

Hydroxyapatite C10[PO4]6[OH]2; 50-60%

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16
Q

What is the primary protein component of bone?

A

Collagen

17
Q

How do the remodeling cycle and serum calcium levels affect one another

A

Decreases bone mass/ increase bone reabsorption = increase calcium in serum

18
Q

Where else is calcium found?

A

Bound to Albumin

19
Q

How is calcium distributed in the serum?

A

Ionized Calcium - 50%
Protein Bound (Albumin) Calcium - 40%
Citrate or Phosphate Bound Calcium - 10%

20
Q

What Factors Regulate the Bone Remodeling Cycle?

A

Serum calcium, hormones, and cytokines

21
Q

What cells are involved in bone remodeling?

A

Osteoblasts Build Bone

Osteoclasts Resorb Bone

22
Q

How do RANK, RANKL, OPG, and Estrogen regulate osteoclasts?

A

Estrogen is a precursor for Osteoprogenerin (OPG).

OPG can bind to RANKL which inhibits it from binding to RANK (this inhibits osteoclasts)

RANKL and RANK binding together will stimulate osteoclasts

23
Q

How do osteoblasts regulate osteoclasts?

A

Osteoblast release RANKL ligand that stimulate RANK receptor and stimulates osteoclast formation

24
Q

What are the major consequences of increased PTH?

A
  1. Increases serum calcium and decreases serum phosphate
  2. Increases calcium reabsorption in the kidneys
  3. Stimulates osteoclasts
  4. Increases absorption in the small intestine
25
Q

What regulates PTH production?

A

Triggered by low plasma Ca levels

26
Q

What are the consequences of increased Vitamin D?

A

Increases serum calcium, increases bone adsorption

27
Q

What regulates Vitamin D Production?

A

Sunlight → precursors synthesized in the skin
Liver = Stores Vitamin D
Kidney = Conversion of Vitamin D to active form occurs

1alpha-hydroxylase is the point of regulation