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Endo/Repro > 05a: Calcium and Parathyroid > Flashcards

05a: Calcium and Parathyroid Flashcards

1
Q

List the three hormones primarily involved in Ca metabolism regulation

A
  1. PTH
  2. 1,25-DHCC (Dihydroxycholecalciferol)
  3. Calcitonin
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2
Q

T/F: 1,25-DHCC is a steroid hormone.

A

True

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3
Q

1,25-DHCC is derived from (X) that primarily functions to (increase/decrease):

A

X = vitamin D
Increase;
Ca absorption from intestine

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4
Q

A (high/low) Ca concentration increases (X) cell excitability. This leads to the condition (Y) tetany.

A

Low;
X = nerve and muscle
Y = hypocalcemic

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5
Q

A (high/low) Ca concentration can cause cardiac arrhythmia and (over-excites/depresses) neuromuscular excitability

A

High;

Depresses

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6
Q

(X)% of Ca is in the skeleton. Normal plasma calcium concentration is:

A

X = 99

10 mg/dL

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7
Q

(X)%, of plasma Ca is bound to plasma proteins. The rest is ultrafiltrable, which means it’s either (Y) or (Z).

A 
X = 40
Y = complexed with anions (PO4)
Z = free, ionized
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8
Q

T/F: Ca that’s complexed with anions (such as PO4) is the biologically active form.

A

False - free, ionized Ca is

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9
Q

T/F: Person taking in 1.0 g Ca means that 0.9 g of it will be absorbed by gut.

A

False - only 0.5 g

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10
Q

T/F: Person taking in 1.0 g Ca means that net gain is about 0.2 g.

A

True - 0.175 g

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11
Q

Net gain of Ca in body is offset by (gain/loss) of (X) in (Y) organ/system. This maintains Ca balance.

A

(Equal) loss;
X = Ca
Y = kidney

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12
Q

List the main sites of important Ca regulation.

A
  1. Bones
  2. Kidney
  3. GI
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13
Q

T/F: Most of the Ca in bones is in a rapidly exchangeable pool.

A

False - only 500 of 25,000 mmol are

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14
Q

(X)% of Ca is reabosrbed in kidney.

A

X = 98

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15
Q

Ca reabsorption in GI tract is via (X) channel/transporter/ATPas.

A

X = Ca-dependent ATPase

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16
Q

Bone is a(n) (X) matrix, impregnated with (Y).

A 
X = collagenous
Y = hydroxyapatites (Ca phosphates)
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17
Q

Bone is both (cellular/acellular) and (well/poorly)-vascularized.

A

Cellular; well-vascularized

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18
Q

The outer layer of (X) bone is (more/less) metabolically active than the inner layer of (Y) bone.

A

X = compact
Less
Y = spongy/trabecular

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19
Q

(X) cells form bone by secreting (Y).

A 
X = osteoblasts
Y = collagen
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20
Q

(X) cells are surrounded by bone matrix and send long processes that ramify throughout bone. They formed from (Y) cells.

A 
X = osteocytes;
Y = osteoblasts (differentiation)
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21
Q

The “bone membrane” separates (X) and (Y) compartments.

A 
X = mineralized bone matrix
Y = ECF (and rest of body)
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22
Q

Bone membrane: what are the components?

A
  1. Endosteum
  2. Periosteum
  3. Osteocytes
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23
Q

Bone resorption is carried out by (X) cells, derived from (Y) cells.

A 
X = osteoclasts
Y = monocyte precursors
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24
Q

Osteoclasts secrete (X) that dissolve (Y) from underlying bone.

A 
X = acids and proteases
Y = mineral crystals and protein matrix
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25
Q

T/F: Osteoclasts and osteoblasts continually communicate with each other via endocrine factors/hormones.

A

False - paracrine factors

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26
Q

Bone: The cytoplasmic processes of (X) cells extend deep into bone and connect to those of (Y) cells via (gap/tight) junctions.

A 
X = osteoblasts;
Y = osteocytes

Gap

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27
Q

UV light acts on (X) compound in skin to produce vitamin D3. Where is vitamin D3 taken?

A

X = 7-dehydrocholesterol

Liver

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28
Q

Vit D synthesis: liver modifies vitamin D3 via (X), forming (Y).

A 
X = hydroxylation
Y = 25OH-D3
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29
Q

The major biologically active form of vitamin D is (X). The final step in its formation occurs in (Y).

A 
X = 1,25-(OH)2-D3
Y = kidney (proximal tubule)
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30
Q

Vit D synthesis: Instead of (X) modification, the kidney could modify 25OH-D3 via (Y), to promote degradation.

A 
X = hydroxylation at 1-position
Y = hydroxylation at 24-position
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31
Q

List the overall, general goals/functions of 1,25-(OH)2-D3.

A

Provide Ca and phosphate to ECF for bone mineralization

32
Q

Vit D deficiency in children causes (X), and in adults causes (Y).

A 
X = rickets
Y = osteomalacia
33
Q

1,25-(OH)2-D3 acts primarily by binding (X) receptor, which (increases/decreases) production of (Y).

A

X = nuclear (VDR, Vitamin D Receptor)
Increases;
Y = CaBP; and Ca and P transporters

34
Q

T/F: Vitamin D Receptor is only present in Ca-regulating tissues.

A

False - wide variety of other tissues as well

35
Q

One method in treating psoriasis uses the mechanism of 1,25-(OH)2-D3 (stimulation/inhibition) of (X) process in cells containing (Y).

A

Inhibition
X = cell proliferation
Y = VDR

36
Q

1,25-(OH)2-D3 (increases/decreases) Ca absorption in GI tract by inducing (increase/decrease):

A 
Increases;
Increase;
1. ECaC (epithelial channels)
2. Calbindin
3. Ca/Na exchangers; Ca pumps
37
Q

T/F: 1,25-(OH)2-D3 directly promotes Ca deposition in bone.

A

False - acts indirectly by increasing plasma Ca and P absorption (their supersaturating levels will promote mineralization)

38
Q

T/F: 1,25-(OH)2-D3 acts indirectly to promote osteoclastic activity and bone resorption.

A

True

39
Q

1,25-(OH)2-D3 acts in synergy with (X), either one being far less effective in (Y) function in absence of the other.

A 
X = PTH
Y = mobilizing Ca stores
40
Q

1,25-(OH)2-D3 acts on proximal nephron to (increase/decrease) (X).

A

Increase;

X = Na-dependent phosphate transporter (thus, increases phosphate reuptake)

41
Q

1,25-(OH)2-D3 acts on distal nephron to (increase/decrease) (X).

A

Increase;

X = ECaC and Calbindin (thus, Ca reabsorption)

42
Q

High plasma concentrations of (X) inhibit 1,25-(OH)2-D3 synthesis (neg-feedback). Specifically, they inhibit (Y).

A 
X = Ca and P; and 1,25-(OH)2-D3
Y = 1a-hydroxylase
43
Q

Synthesis of 1a-hydroxylase enzyme is prompted by (high/low) levels of PTH and (high/low) levels of P.

A

High; low

44
Q

1,25-(OH)2-D3 feedback/regulation: (X) stimulates (Y) enzyme to produce (Z), leading to degradative pathway.

A 
X = 1,25-(OH)2-D3
Y = 24-hydroxylase
Z = 24,25-(OH)2-D3
45
Q

(X) cells in the parathyroid make PTH. The hormone is synthesized as (Y) and undergoes (Z) modification to become “mature” PTH.

A 
X = chief/principal
Y = pre-pro-hormone
Z = cleavage
46
Q

T/F: Half-life of intact PTH is about 30 min.

A

False - 5 min

47
Q

T/F: PTH is rapidly cleaved/degraded in peripheral tissues.

A

False - in Kupfer cells in liver

48
Q

Primary signal that stimulates PTH secretion is (X).

A

X = low circulating Ca levels

49
Q

Ca Sensing Receptor (CaSR) is found in (X) cells. It functions to:

A

X = parathyroid chief

Monitor extracellular Ca levels

50
Q

By default, PTH is (secreted/stored) in/from (X) cells until (Y).

A

Secreted;
X = chief
Y = high Ca levels bind CaSR, which activates pathway to inhibit PTH secretion

51
Q

T/F: Like 1,25-(OH)2-D3, PTH acts to increase serum Ca and PO4.

A

False - increase serum Ca, but decrease serum PO4

52
Q

PTH acts by activating (X) receptor, leading to (production/cleavage) of (Y).

A

X = G-protein
Production
X = cAMP and IP3

53
Q

List the 5 general actions of PTH.

A
  1. Increase bone resoprtion/Ca mobilization
  2. Increase Ca reabsorption (kidney)
  3. Decrease plasma PO4
  4. Increase 1,25-(OH)2-D3 production
  5. Increase osteoclast and osteoblast formation
54
Q

PTH will (increase/decrease) serum PO4 via which mechanism?

A

Decrease;

Increase urine PO4 excretion (decreases proximal tubule reabsorption)

55
Q

T/F: PTH acts directly on intestine to increase Ca reabsorption.

A

False - indirect by stimulating 1,25-(OH)2-D3 formation

56
Q

Bone: (X) compounds stimulate the expression of RANKL on surface of (Y) cells. This interacts with (Z).

A 
X = PTH and 1,25-(OH)2-D3
Y = osteoblasts
Z = RANK (receptor) on (pre)osteoclasts
57
Q

T/F: Increasing RANKL expression on osteoblasts will decrease bone resorption.

A

False - RANKL activates osteoclasts (via binding RANK receptor)

58
Q

(X) hormones are important regulators of bone resorption. They enhance (Y) production, which acts as decoy by binding/blocking (RANK/RANKL).

A 
X = estrogens
Y = Osteoprotegerin (OPG)

RANKL (prevents RANK activation)

59
Q

T/F: PTH has a short-term anabolic effect, by increasing osteoblast activity.

A

True (but limited)

60
Q

Pulsatile injections of (X) is used clinically to treat osteoporosis. The pulsatile nature functions to sidestep (Y).

A 
X = PTH
Y = osteoblast apoptosis (via prolonged PTH stimulation)
61
Q

Specific action of PTH on proximal nephron: (increase/decrease) (X) activity, which (increases/decreases) (Y) formation and excretion.

A

Increase;
X = AC
Increases;
Y = cAMP (thus, phosphate)

62
Q

(High/low) urinary levels of (X) is often used as an index of excess PTH secretion.

A

High;

X = cAMP

63
Q

Severe (increases/decreases) in Mg levels inhibit PTH production.

A

Both!

64
Q

PTH regulation: (X) acts directly on parathyroid to decrease PTH secretion.

A

X = Ca

65
Q

PTH regulation: (X) acts directly on parathyroid to decrease PTH precursor production.

A

X = 1,25-(OH)2-D3

66
Q

Chronic kidney disease likely leads to (hyper/hypo)-parathyroidism. Why?

A

Hyperparathyroidism (due to low 1,25-(OH)2-D3 formation and low Ca reabsorption)

67
Q

Parathyroidectomy will lead to (increase/decrease) in plasma concentrations of (X).

A

Increase (X = PO4); Decrease (X = Ca)

68
Q

T/F: PTH is essential for life.

A

True

69
Q

You’d expect to see Ca-containing stones in PTH (deficiency/excess).

A

Excess

70
Q

PTH-related peptide (PTHrP) is found in plasma of some patients. What are its actions? Serum PTH levels would (increase/decrease) in presence PTHrP.

A

All same physiological actions of PTH;

Decrease (result of hypercalcemia)

71
Q

Calcitonin is produced by (X) cells in presence of (high/low) levels of (Y).

A

X = parafollicular cells (in thyroid)
High;
Y = Ca

72
Q

Calcitonin (increases/decreases) Ca permeability in osteoclasts/osteoblasts, thus (increasing/decreasing) plasma Ca and PO4.

A

Decreases;

decreasing

73
Q

The biological activity of PTH is dictated mainly by the (X) portion of the molecule.

A

X = N-terminal

74
Q

The main circulating form of vitamin D3 is (X). And most is (bound/unbound).

A

X = 25-hydroxyvitamin D3

Bound (to Vit DBP)

75
Q

T/F: High PTH levels may lead to osteomalacia.

A

False - PTH stimulates 1a-hydroxylase

76
Q

High plasma FGF23 would (stimulate/inhibit) 1a-hydroxylase and (increases/decreases) chance of osteomalacia.

A

Inhibit;

increases

Endo/Repro (15 decks)

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