Test 3 - Schricker Flashcards

(27 cards)

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?

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
What regulates PTH production?
Triggered by low plasma Ca levels
26
What are the consequences of increased Vitamin D?
Increases serum calcium, increases bone adsorption
27
What regulates Vitamin D Production?
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