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Endo/Repro Exam 1 > Parathyroid Hormone, Calcitonin, and VItamin D > Flashcards

Parathyroid Hormone, Calcitonin, and VItamin D Flashcards

1
Q

What is cortical bone?

A

Compact bone that forms the cortex or outer shell of most bones

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2
Q

What is the medullary cavity?

A

Central cavity of bone shafts where red bone marrow and or yellow bone marrow

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3
Q

What is osteoid?

A

Provides sites for nucleation of hydroxyapatite crystals

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4
Q

What is the main protein in osteoid?

A

Type I collagen

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5
Q

What is the fundamental functional unit of compact bone?

A

Osteon or Haversion system

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6
Q

When it comes to metabolic function versus structural function of bone what has priority?

A

Metabolic to maintain homeostasis

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7
Q

What does absence of weight-bearing lead to?

A

Promotes demineralization of bone leading to increased plasma Ca2+ levels, decreased PTH, increased urinary Ca2+

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8
Q

What is the large bulge of osteoblastic tissue and new bone formation at the point of a break called?

A

Callus

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9
Q

What does alkalosis cause?

A

Decreases free Ca plasma levels

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10
Q

What does acidosis cause?

A

Increased free Ca plasma levels

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11
Q

How does alkalosis and acidosis affect calcium?

A

Be baring the amount bound to proteins

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12
Q

What are the forms of Ca2+ found in plasma?

A

Ionized Ca2+
Protein-bound Ca2+
Calcium complexed to anions

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13
Q

What does hypocalcaemia lead to?

A

Neuron depolarizing spontaneously that can lead to tetany and seizures

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14
Q

What does hypercalcemia cause?

A

Depresses the nerve and muscle activity,
Sluggish CNS and reflexes, Decreased QT
Lack of appetite
Constipation

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15
Q

When does bone deposition occur?

A

When [Ca2+] x [PO4-] > solubility product

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16
Q

When [Ca] is elevated what sensor is activated?

A

Calcium-sensing receptors (PT gland)

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17
Q

What are calcium-sensing receptors and what do they do?

A

G-protein (q) receptors that bind extracellular calcium; increased calcium binding to the receptors activates Gq (PIP2-> IP3 and DAG) the calcium released intracellularly will lead to calcium inhibiting fusion and release of PTH from vesicles

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18
Q

What effect does vitamin D have on PTH?

A

Inhibits PTH transcription

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19
Q

How does vitamin D mediate its effects on PTH?

A

Binds Vit-D-VDR to the VDR response element leading to decreased rate of PTH transcription

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20
Q

What cell in the PT gland releases PTH?

A

Chief cells

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21
Q

What is the stronger stimulus for calcium regulation in adults?

A

PTH not calcitonin

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22
Q

What causes familial hypercalcemic hypocalciuria?

A

Ca receptor in patients is mutated resulting in [Ca] being higher than normal

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23
Q

What occurs in FHH?

A

Calcium levels must be higher in the plasma before inhibiting PTH secretion resulting in normal PTH but elevated [Ca]

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24
Q

Mode of inheritance in FHH?

A

Autosomal dominant disorder

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25
Q

What drug is used for parathyroid cancer and hyperparathyroidism?

A

Calcimetrics

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26
Q

How does calcimetrics work?

A

It is a CaSR agonist mimicking Calcium

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27
Q

What is the key action of PTH?

A

Promote Ca reabsorption in TAL and DCT

Reduce reabsorption of PO4 in PCT and DCT

28
Q

What inhibits osteoclast action?

A

Calcitonin

Estrogen

29
Q

What is the PTH-1R coupled to?

A

Both Gs and Gaq receptors

30
Q

Effect of PTH-1R Gaq when stimulated?

A

Reduces Pi absorption

31
Q

Effect of Gs coupled with PTH-1R?

A

Secretion of M-CSF/RANK-L/IL-6 by osteoblasts

32
Q

What does M-CSF (macrophage colony stimulating factor) cause?

A

Osteoclast precursors to proliferate and form mature multinucleated osteoclasts

33
Q

What does RANK-L protein cause?

A

Stimulated pre-osteoclasts to become osteoclasts

34
Q

What do glucocorticoids increase the production of in osteoblasts?

A

RANK-L

35
Q

What proteins are needed for osteoclasts to attach to bone matrix?

A

Integrin on the membrane attach to vitronectin in bone matrix

36
Q

What inhibits differentiation of osteoclast precursor into mature osteoclasts?

A

Osteoprotegrin

37
Q

What is osteoprotegrin?

A

A decoy receptor for RANK-L

38
Q

What is tartrate-resistant acid phosphatase (TRAP)?

A

Decreases osteoclast activity (mechanism not known) causing osteopetrosis (thick brittle bones)

39
Q

Three main effects of PTH?

A
  1. ) Promotes Ca2+ reabsorption
  2. ) Inhibits PO43- reabsorption
  3. ) Promotes hydroxylation of 25-hydroxyviatmin D activating vitamin D
40
Q

PTH half-life:

A

1-84 PTH rapidly cleared by kidneys

Smaller fragments have full activity and takes several hours

41
Q

What does vitamin D directly cause on bone?

A

Bone demineralization (breakdown)

42
Q

How does vitamin D indirectly cause deposition of bone?

A

It causes Ca/PO4 reabsorption from both smooth muscle and the kidney raising Ca/PO4 plasma levels and causing deposition in bones (deposition overshadows the bone demineralization by the direct affect of vitamin D)

43
Q

What does Ca2+ and PO4 ingestion cause in PTH and Vit D respectively?

A

Ca: PTH and Vit D decrease
PO4: PTH and Vit D increase

44
Q

What does increased phosphorus ingestion cause?

A

Lower Ca levels and increase Ca/PO4 ratio promoting bone mineralization

45
Q

What cells secrete calcitonin?

A

C cells (parafollicular cells) in the thyroid

46
Q

Cellular mechanism of calcitonin action?

A

Receptors on osteoclasts are coupled to both cAMP-PKA and Ca2+ PKC mediated signaling pathways

47
Q

CT effect on osteoclasts?

A

Decreased activity decreasing bone reabsorption

48
Q

What diseases is CT useful in treating?

A

Paget’s disease
Severe hypercalcemia
Osteoporosis

49
Q

Four ways calcitonin lowers blood Ca2+ levels:

A
  1. ) Inhibits Ca2+ absorption in intestines
  2. ) Inhibits osteoclast activity
  3. ) Stimulates osteoblast activity
  4. ) Inhibits renal tubular reabsorption of Ca2+
50
Q

CT half-life?

A

50-80 minutes; degraded in the kidneys

51
Q

What is PTHrP?

A

PTH-related peptide (they don’t know anything about it really)

52
Q

Where is PTHrP synthesized?

A

In normal and malignant tissues

53
Q

What does PTHrP receptor in kidney and bone cause?

A

Produces the actions of PTH aka hypercalcemia

54
Q

When is PTHrP released?

A

In lactating breast to promote mobilization of calcium from maternal bone during milk production

55
Q

What causes rickets?

A

Vitamin D deficiency in children causing reduced rigidity of bones and bowing of long bones

56
Q

What is osteomalacia?

A

Vitamin D deficiency in adults leading to brittle bones but not bowing of long bones

57
Q

Why does bowing of long bones occur in rickets but not osteomalacia?

A

Because rickets is in children before closure of their growth plates where osteomalacia only occurs in adults after the closure of growth plates

58
Q

What is osteoporosis?

A

Loss of bone mass and density

59
Q

What is osteopetrosis?

A

Increase in bone mass and density

60
Q

What causes osteopetrosis?

A

Malfunctioning in osteoclasts resulting in a deficiency in carbonic anhydrase encoded by the gene CA2 (needed for breakdown of bone)

61
Q

What is Paget’s disease?

A

Excessive breakdown and formation of bone leading to disorganized bone remodeling

62
Q

What bones does Paget’s disease affect?

A

Pelvis, femur, lumbar vertebrae

63
Q

What is the first manifestation of Paget’s disease?

A

Elevated alkaline phosphatase in blood

64
Q

What is seen in the facial bones of Paget’s disease?

A

Grossly over thickening and deformation

65
Q

What is affected in FHH?

A

Mutation in Ca2+ receptor on PT chief cells

Endo/Repro Exam 1 (17 decks)

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